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Introduction: Brain ischemia-reperfusion can cause serious and irreversible health problems. Recent studies have suggested that certain flavonoids may help stabilize the correctly folded structure of the visual photoreceptor protein rhodopsin and offset the deleterious effect of retinitis pigmentosa mutations., Objective: The current study aimed to determine the effect of 3',4'-Dihydroxyflavonol (DiOHF) supplementation for 1 week on lipid peroxidation in the retina tissue following focal brain ischemia-reperfusion in rats., Methods: This study was carried out on male Wistar-albino rats. A total of 28 rats were used in the research, and four groups were formed: Control group: no anesthesia or surgical procedure was applied to the animals in this group, Sham group: after general anesthesia was established in the animals in this group, the carotid artery areas were opened and closed, and the 1 ml vehicle was applied for 1 week, Ischemia-Reperfusion (I/R) group: after the carotid arteries were isolated in rats under general anesthesia, ischemia was performed by ligating them for 30 minutes, and then reperfusion was applied for 1 week, and Ischemia-Reperfusion + DiOHF group: under general anesthesia, ischemia was developed in the carotid arteries of the rats by ligation for 30 minutes, and then DiOHF was applied along with reperfusion for 1 week. At the end of the study, retinal tissue taken from animals sacrificed under general anesthesia was analyzed for MDA and GSH. Retinal tissue was also examined for histology and neurogenesis., Results: The highest MDA value was determined in the ischemia group, and the lowest value in the control and sham groups. In group 4, this parameter was found to be significantly lower than in the I/R group. Retinal GSH was very low in the I/R group. However, 1-week DiOHF treatment increased the GSH values. Deteriorations also occurred in the histological structure of the retinal tissue, and neurogenesis was inhibited. However, treatment improved retinal damage and neurogenesis., Conclusion: The results of the current study showed that focal brain ischemia in rats caused significant retinal lipid peroxidation. However, 1-week DiOHF treatment suppressed the increased lipid peroxidation by increasing GSH levels. Moreover, treatment improved retinal damage and neurogenesis., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The aim of this study was to investigate the effects of dietary zinc status on spinal cord tissue damage and ZnT3, IL-6 gene expressions in a cuprizone-induced rat Multiple Sclerosis (MS) model. The study was carried out on 46 adult male rats of the genus Wistar. The animals used in the study were divided into 5 groups (G) (Control 6, other groups 10). G1, Control. G2, Sham-MS: Carboxy-methyl-cellulose (KMS) solution in which Cuprizon was dissolved was given to rats by gavage daily for 8 weeks at the rate of 1 % of daily feed consumption. MS was formed by giving 1 % of the daily feed consumption cuprizon in KMS solution by gavage to the animals in G3, 4 and 5 for 8 weeks. G4 was fed with a zinc deficient (50 µg/kg zinc) diet. G5 was given intraperitoneal (ip) zinc sulfate (5 mg/kg/day) supplementation. MS formation in animals was determined by Rotarod tests and Myelin Basic Protein (MBP) gene expression analysis. ZNT3 and IL-6 gene expression levels in spinal cord tissue samples of animals by Real-Time-PCR method; MDA and GSH levels were determined by ELISA method. The highest spinal cord MDA and IL-6 levels were obtained in G3 and G4 (P<0.05). Zinc supplementation in G5 prevented the increase in the mentioned parameters and turned them into control values (P<0.05). The spinal cord GSH and ZnT3 levels of G3 and G4 were lower than all other groups (P<0.05). Zinc supplementation prevented suppression in the same parameters in G5 and reached the control values (P<0.05). The findings of the current study suggest that zinc supplementation in addition to treatment for MS may be beneficial in reducing the severity of the disease., Competing Interests: Declaration of Competing Interest The authors declare that they have no potential conficts of interest to disclose., (Copyright © 2024 Elsevier GmbH. All rights reserved.)

Objective: Ischemic stroke is the leading cause of mortality and disability worldwide with more than half of survivors living with serious neurological sequelae thus, it has recently attracted considerable attention in the field of medical research. Neurogenesis is the process of formation of new neurons in the brain, including the human brain, from neural stem/progenitor cells [NS/PCs] which reside in neurogenic niches that contain the necessary substances for NS/PC proliferation, differentiation, migration, and maturation into functioning neurons which can integrate into a pre-existing neural network.Neurogenesis can be modulated by many exogenous and endogenous factors, pathological conditions. Both brain-derived neurotrophic factor, and flavonoids can modulate the neurogenic process in physiological conditions and after various pathological conditions including ischemic insults., Aim: This review aims to discuss neurogenesis after ischemic insults and to determine the role of flavonoids and BDNF on neurogenesis under physiological and pathological conditions with a concentration on ischemic insults to the brain in particular., Method: Relevant articles assessing the impact of flavonoids and BDNF on neurogenic processes in various physiological/pathological conditions including ischemic insults within the timeline of 1965 until 2023 were searched using the PubMed database., Conclusions: The selected studies have shown that ischemic insults to the brain induce NS/PC proliferation, differentiation, migration, and maturation into functioning neurons integrating into a pre-existing neural network. Flavonoids and BDNF can modulate neurogenesis in the brain in various physiological/pathological conditions including ischemic insults. In conclusion, flavonoids and BDNF may be involved in post-ischemic brain repair processes through enhancing endogenous neurogenesis.

Introduction: Ischemia/reperfusion is a pathological condition by the restoration of perfusion and oxygenation following a period of restricted blood flow to an organ. To address existing uncertainty in the literature regarding the effects of 3', 4'-dihydroxy flavonol (DiOHF) on cerebral ischemia/reperfusion injury, our study aims to investigate the impact of DiOHF on neurological parameters, apoptosis (Caspase-3), aquaporin 4 (AQP4), and interleukin-10 (IL-10) levels in an experimental rat model of brain ischemia-reperfusion injury., Materials/methods: A total of 28 Wistar-albino male rats were used in this study. Experimental groups were formed as 1-Control, 2-Sham, 3-Ischemia-reperfusion, 4-Ischemia-reperfusion + DiOHF (10 mg/kg). The animals were anaesthetized, and the carotid arteries were ligated (ischemia) for 30 min, followed by reperfusion for 30 min. Following reperfusion, DiOHF was administered intraperitoneally to the animals at a dose of 10 mg/kg for 1 week. During the one-week period neurological scores and new object recognition tests were performed. Then, caspase 3 and AQP4 levels were determined by PCR method and IL-10 by ELISA method in hippocampus tissue samples taken from animals sacrificed under anaesthesia., Results: Brain ischemia reperfusion significantly increased both caspase 3 and AQP4 values in the hippocampus tissue, while decreasing IL-10 levels. However, 1-week DiOHF supplementation significantly suppressed increased caspase 3 and AQP4 levels and increased IL-10 values. While I/R also increased neurological score values, it suppressed the ability to recognize new objects, and the administered treatment effectively ameliorated the adverse effects observed, resulting in a positive outcome., Conclusions: The results of the study show that brain ischemia caused by bilateral carotid occlusion in rats and subsequent reperfusion causes tissue damage, but 1-week DiOHF application has a healing effect on both hippocampus tissue and neurological parameters., Competing Interests: Declaration of competing interest Authors state no conflict of interest., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The present study aimed to determine the effect of 3',4'-dihydroxyflavonol (DiOHF) on apoptosis in the cerebellum and hippocampus in rats with ischemia-reperfusion. A total of 38 Wistar albino male rats were used. Experimental groups were designed as Group 1-Sham; Group 2-Ischemia-reperfusion (IR), in which animals were anesthetized and carotid arteries ligated for 30 minutes (ischemia) and reperfused 30 minutes; Group 3- IR + DiOHF (10 mg/kg); Group 4- Ischemia + DiOHF (10 mg/kg) + reperfusion; Group 5-DiOHF + IR. DiOHF was supplemented as 10 mg/kg by intraperitoneal injection 30 minutes before IR. Following application, the animals were sacrificed under general anesthetic by cervical dislocation, and the cerebellum and hippocampus tissues were analyzed for apoptosis. IR significantly increased hippocampus and cerebellum apoptosis activity, confirmed by Hematoxylin-Eosin, TUNEL labeling, and Caspase-8 activity. However, these values were significantly suppressed by the administration of DiOHF, especially when used before the ischemia and reperfusion. The results of the study show that increased apoptosis in the cerebellum and hippocampus tissue was inhibited by intraperitoneal DiOHF supplementation.

The aim of this study was to investigate how zinc deficiency and supplementation affect liver markers including autotaxin, kallistatin, endocan, and zinc carrier proteins ZIP14 and ZnT9 in rats exposed to maternal zinc deficiency. Additionally, the study aimed to assess liver tissue damage through histological examination. A total of forty male pups were included in the research, with thirty originating from mothers who were given a zinc-deficient diet (Groups 1, 2, and 3), and the remaining ten born to mothers fed a standard diet (Group 4). Subsequently, Group 1 was subjected to a zinc-deficient diet, Group 2 received a standard diet, Group 3 received zinc supplementation, and Group 4 served as the control group without any supplementation. Upon completion of the experimental phases of the study, all animals were sacrificed under general anesthesia, and samples of liver tissue were obtained. The levels of autotaxin, kallistatin, endocan, ZIP 14, and ZnT9 in these liver tissue samples were determined using the ELISA technique. In addition, histological examination was performed to evaluate tissue damage in the liver samples. In the group experiencing zinc deficiency, both endocan and autotaxin levels increased compared to the control group. With zinc supplementation, the levels of endocan and autotaxin returned to the values observed in the control group. Similarly, the suppressed levels of kallistatin, ZIP14, and ZnT9 observed in the zinc deficiency group were reversed with zinc supplementation. Likewise, the reduced levels of kallistatin, ZIP14, and ZnT9 seen in the zinc deficiency group were rectified with zinc supplementation. Moreover, the application of zinc partially ameliorated the heightened liver tissue damage triggered by zinc deficiency. This study is the pioneering one to demonstrate that liver tissue dysfunction induced by a marginal zinc-deficient diet in rats with marginal maternal zinc deficiency can be alleviated through zinc supplementation., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Ischemic stroke is the leading cause of mortality and disability worldwide with more than half of survivors living with serious neurological sequelae; thus, it has recently attracted a lot of attention in the field of medical study., Purpose: The aim of this study was to determine the effect of naringin supplementation on neurogenesis and brain-derived neurotrophic factor (BDNF) levels in the brain in experimental brain ischemia-reperfusion., Study Design: The research was carried out on 40 male Wistar-type rats (10-12 weeks old) obtained from the Experimental Animals Research and Application Center of Selçuk University. Experimental groups were as follows: (1) Control group, (2) Sham group, (3) Brain ischemia-reperfusion group, (4) Brain ischemia-reperfusion + vehicle group (administered for 14 days), and (5) Brain ischemia-reperfusion + Naringin group (100 mg/kg/day administered for 14 days)., Methods: In the ischemia-reperfusion groups, global ischemia was performed in the brain by ligation of the right and left carotid arteries for 30 min. Naringin was administered to experimental animals by intragastric route for 14 days following reperfusion. The training phase of the rotarod test was started 4 days before ischemia-reperfusion, and the test phase together with neurological scoring was performed the day before and 1, 7, and 14 days after the operation. At the end of the experiment, animals were sacrificed, and then hippocampus and frontal cortex tissues were taken from the brain. Double cortin marker (DCX), neuronal nuclear antigen marker (NeuN), and BDNF were evaluated in hippocampus and frontal cortex tissues by Real-Time qPCR analysis and immunohistochemistry methods., Results: While ischemia-reperfusion increased the neurological score values, DCX, NeuN, and BDNF levels decreased significantly after ischemia in the hippocampus and frontal cortex tissues. However, naringin supplementation restored the deterioration to a certain extent., Conclusion: The results of the study show that 2 weeks of naringin supplementation may have protective effects on impaired neurogenesis and BDNF levels after brain ischemia and reperfusion in rats., (© 2024. The Author(s).)

Background: Microvascular dysfunction develops in tissues after Ischemia-Reperfusion (IR). The current study aimed to determine the effect of naringin supplementation on kidney caspase-3, IL-1β, and HIF-1α levels and kidney histology in rats undergoing unilateral nephrectomy and kidney-ischemia reperfusion., Methods: The study was conducted on 8-12 weeks old 40 Wistar-type male rats. Experimental renal ischemia- reperfusion and unilateral nephrectomy were performed under general anesthesia in rats. Experimental groups were formed as follows: 1-Control group, 2-Sham control + Vehicle group, 3- Renal ischemia-reperfusion (Renal I+R) + Vehicle group, 4-Renal I+R + Naringin (50 mg/kg/day) group (3 days application) group, 5-Renal I+R + Naringin (100 mg/kg/day) group (3 days supplementation). Nephrectomy in the left kidneys and the ischemia for 45 minutes and reperfusion in the right kidneys followed by 72 hours of reperfusion. Naringin was administered intraperitoneally at the beginning of the reperfusion, 24 hours and 48 hours later. At the end of the experiments, blood was first taken from the heart in animals under general anesthesia. Then, the animals were killed by cervical dislocation, and kidney tissue samples were taken. Tissues were evaluated for caspase-3, IL-1β, and HIF-1α as well as histologically., Results: As a result of ischemia in kidney tissues, HIF-1α decreased, while caspase-3 and IL-1β increased. IR also caused damage to the kidney tissue. However, naringin supplementation corrected the deterioration to a certain extent., Conclusion: The results of the study showed that naringin may have protective effects on kidney damage due to anti-inflammatory and antiapoptosis mechanisms caused by unilateral nephrectomy and IR in rats., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objectives: The aim of this study was to investigate how melatonin administration affects retinal oxidative damage and retinal SIRT1 gene activation in diabetic elderly female rat model., Methods: 16-months-old female rats were used in the study. A total of 24 rats were divided into 4 groups in equal numbers: Group 1. Control, Group 2. Control + Melatonin, Group 3. Diabetes, Group 4. Diabetes + Melatonin. In group 3 and 4 rats, diabetes was induced by intraperitoneal (IP) injection of streptozotocin. Groups 2 and 4 were given ip melatonin for 4 weeks. SIRT-1 gene expression was determined by PCR method and GSH and MDA levels by ELISA in retinal tissue samples taken from animals sacrificed under general anesthesia., Results: In our study, the highest retinal SIRT1 expression values were obtained in the diabetes + melatonin (G4) group. The retinal SIRT1 expression values of the diabetes group (G3) were lower than group 4 and higher than the general control (G1) and control + melatonin (G2) groups. Again in our study, the highest retinal MDA values were obtained in the diabetes group (G3). The highest retinal GSH values were obtained in the Diabetes + melatonin group (G4)., Conclusion: The results of our study showed that melatonin supplementation has a protective effect on retinal tissue in a diabetic elderly female rat model. This protective effect of melatonin supplementation occurs by increasing both retinal antioxidant activity and retinal SIRT1 gene expression., Competing Interests: Declaration of Competing Interest The authors declare that they have no potential conficts of interest to disclose., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Objectives: Zinc, which is found in high concentrations in the β-cells of the pancreas, is also a critical component for the endocrine functions of the pancreas. SLC30A8/ZnT8 is the carrier protein responsible for the transport of zinc from the cytoplasm to the insulin granules. The aim of this study was to investigate how dietary zinc status affects pancreatic beta cell activation and ZnT8 levels in infant male rats born to zinc-deficient mothers., Methods: The study was performed on male pups born to mothers fed a zinc-deficient diet. A total of 40 male rats were divided into 4 equal groups. Group 1: In addition to maternal zinc deficiency, this group was fed a zinc-deficient diet. Group 2: In addition to maternal zinc deficiency, this group was fed a standard diet. Group 3: In addition to maternal zinc deficiency, this group was fed a standard diet and received additional zinc supplementation. Group 4: Control group. Pancreas ZnT8 levels were determined by ELISA method and insulin-positive cell ratios in β-cells by immunohistochemistry., Results: The highest pancreatic ZnT8 levels and anti-insulin positive cell ratios in the current study were obtained in Group 3 and Group 4. In our study, the lowest pancreatic ZnT8 levels were obtained in Group 1 and Group 2, and the lowest pancreatic anti-insulin positive cell ratios were obtained in Group 1., Conclusion: The results of the present study; in rats fed a zinc-deficient diet after maternal zinc deficiency has been established shows that ZnT8 levels and anti-insulin positive cell ratios in pancreatic tissue, which is significantly suppressed, reach control values with intraperitoneal zinc supplementation., Competing Interests: Declaration of Competing Interest The authors declare that they have no potential conficts of interest to disclose., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Metabolic dysfunction is a critical step in the etiopathogenesis of Alzheimer's disease. In this progressive neurological disorder, impaired zinc homeostasis has a key role that needs to be clarified. The aim of this study was to investigate the effect of zinc deficiency and administration on hippocampal Nogo-A receptor and osteocalcin gene expression in rats injected with intracerebroventricular streptozotocin (icv-STZ). Forty male Wistar rats were divided into 5 groups in equal numbers: Sham 1 group received icv artificial cerebrospinal fluid (aCSF); Sham 2 group received icv a CSF and i.p. saline; STZ group received 3 mg/kg icv STZ; STZ-Zn-deficient group received 3 mg/kg icv STZ and fed a zinc-deprived diet; STZ-Zn-supplemented group received 3 mg/kg icv STZ and i.p. zinc sulfate (5 mg/kg/day). Hippocampus tissue samples were taken following the cervical dislocation of the animals under general anesthesia. Nogo-A receptor and osteocalcin gene expression levels were determined by real-time-PCR method. Zinc supplementation attenuated the increase in hippocampal Nogo-A receptor gene expression, which was significantly increased in zinc deficiency. Again, zinc supplementation upregulated the intrinsic protective mechanisms of the brain by activating osteocalcin-expressing cells in the brain. The results of the study show that zinc has critical effects on Nogo-A receptor gene expression and hippocampal osteocalcin gene expression levels in the memory-sensitive rat hippocampus that is impaired by icv-STZ injection. These results are the first to examine the effect of zinc deficiency and supplementation on hippocampal Nogo-A receptor and osteocalcin gene expression in icv-STZ injection in rats., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background/Purpose: This research was performed to determine the effect of naringenin (NAR) in experimental hyperuricemia (HU) induced by potassium oxonate (PO) on uric acid levels and xanthine oxidase (XO), inflammation, apoptotic pathway, DNA damage, and antioxidant system in kidney tissue. Study Design: Wistar Albino rats were categorized into four groups: (1) Control group, (2) PO group, (3) [PO+NAR] (2 weeks) group, and (4) PO (2 weeks)+NAR (2 weeks) group. Methods: The first group was not administered any drug. In group 2, PO was administered intraperitoneally 250 mg/kg/day for 2 weeks. In the third group, 100 mg/kg/day NAR was given intraperitoneally 1 hr after PO injection for 2 weeks. In the fourth group, PO was injected for the first 2 weeks, followed by NAR injection for the second 2 weeks. Serum uric acid levels, XO, nuclear factor-kappa B, tumor necrosis factor-alpha, interleukin-17, cytochrome c, 8-Hydroxydeoxyguanosine (8-OHdG), glutathione peroxidase (GPx), and caspase-3 levels in kidney were determined. Results: HU increased the levels of inflammatory and apoptotic parameters, XO, and 8-OHdG levels in kidney. Administration of NAR caused a decrease in these values and an increase in GPx levels. Conclusions: The results of the study show that NAR treatment reduces serum uric acid levels, and apoptosis, inflammation, and DNA damage; increases antioxidant activity in kidney in experimental HU.

We aimed to investigate the effects of melatonin and resveratrol on diabetes-related papillary muscle dysfunction and structural heart disorders. The protective effect of resveratrol and melatonin supplementation on cardiac functions was investigated in a diabetic elderly female rat model. 16-month-old rats (n=48) were allocated into 8 groups. Group1: Control, Group2: Resveratrol Control, Group3: Melatonin Control, Group4: Resveratrol and Melatonin Control, Group5: Diabetes, Group6: Diabetes Resveratrol, Group7: Diabetes Melatonin, Group8: Diabetes Resveratrol and Melatonin. Streptozotocin was injected intraperitoneally to the rats for experimental diabetes induction. Thereafter, resveratrol (intraperitoneal) and melatonin (subcutaneous) were administered for 4 weeks. Resveratrol and melatonin had a protective effect on the contractile parameters and structural properties of the papillary muscle, which was impaired by diabetes. it has been presented that diabetes impairs the contractile function of the papillary muscle for each stimulus frequency tested and the responses obtained as a result of Ca+2 uptake and release mechanisms from the Sarcoplasmic reticulum, and it has been observed that these effects are improved with resveratrol and melatonin injection. The decrease in myocardial papillary muscle strength in the diabetic elderly female rat can be reversed with the combination of resveratrol, melatonin and resveratrol+melatonin. Melatonin+resveratrol supplementation is no different from melatonin and/or resveratrol supplementation. Resveratrol and melatonin supplementation may have a protective effect on cardiac functions in a diabetic elderly female rat model.

We aimed to examine the effects of brain ischemia-reperfusion (IR) especially on serum parameters or liver enzymes, free radicals, cytokines, oxidatively damaged DNA, spermidine/spermine N-1-acetyltransferase (SSAT). The effects of addition of putrescine on IR will be evaluated in terms of inflammation and oxidant-antioxidant balance in liver.The study was conducted on 46 male Albino Wistar rats weighing 200-250 g. The rats were grouped into: 1-Sham group (n = 6). 2-IR group (n = 8): The carotid arteries were ligated for 30-min and reperfusion was achieved for 30-min under general anesthesia. 3-Ischemia + putrescine + reperfusion group (IPR) (n = 8): Unlike the IR group, a single dose of 250 μmol kg-1 putrescine was given by gavage at the beginning of reperfusion. In putrescine treatment groups in addition to the procedures performed in the IR group a total of 4 doses of 250 μmol kg-1 putrescine were given at 12-h intervals, with the first dose immediately after 30-min reperfusion (4-IR+putrescine group (IR+P1) (n = 8)); 3 h after the 30-min reperfusion (5-IR+putrescine group (IR+P2) (n = 8)); 6 h after the 30-min reperfusion (6-IR+putrescine group (IR+P3) (n = 8)). ALT, AST, ATP, NO, SSAT, 8-OHdG levels were analyzed in the serum, and liver samples. NF-κB and IL-6 levels were analyzed in the liver samples.Brain IR causes inflammatory, oxidative and DNA damage in the liver, and putrescine supplementation through gavage reduces liver damage by showing anti-inflammatory and antioxidant effects.

The roles of melatonin and resveratrol-enhanced activation of SIRT1 (silent information regulator 1), GLUT4 (glucose transporter type 4), and PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha) in mediating the protective effects on the heart in aged female rats with streptozotocin-induced diabetes were investigated. 16-month-old 48 Wistar female rats were separated into 8 groups with equal numbers. Group 1: Control, Group 2: Resveratrol Control, Group 3: Melatonin Control, Group 4: Resveratrol and Melatonin Control, Group 5: Diabetes, Group 6: Diabetes Resveratrol, Group 7: Diabetes Melatonin, Group 8: Diabetes Resveratrol and Melatonin. A single dose of 40 mg/kg intraperitoneal streptozotocin was injected into the rats of Groups 5, 6, 7, and 8 to induce experimental diabetes. Blood glucose levels were measured from the tail veins of the animals six days after the injections, using a diagnostic glucose kit. Rats with a blood glucose levels ≥300 mg/dl were considered diabetic. 5 mg/kg/day of resveratrol (intraperitoneal) and melatonin (subcutaneous) were administered for four weeks. At the end of the applications, SIRT1, GLUT4, PGC-1α gene expression as well as MDA and GSH levels in the heart tissues were determined by the PCR method from heart tissue samples taken under general anesthesia. The findings of our study show that suppressed antioxidant activity and decreased GLUT4, SIRT1, and PGC-1α gene expression in heart tissue can be reversed by the combination of resveratrol, melatonin, and resveratrol + melatonin in a diabetic aged female rat model. Resveratrol and melatonin supplementation may have a protective effect on cardiac functions in the diabetic aged female rat model., Competing Interests: Conflict of interest The authors declare that they have no potential conflicts of interest to disclose., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Irisin is a thermogenic hormone that leads to causes energy expenditure by increasing brown adipose tissue (BAT). This protein hormone that enables the conversion of white adipose tissue (WAT) to BAT is the irisin protein. This causes energy expenditure during conversion. WAT stores triglycerides and fatty acids and contains very few mitochondria. They also involve in the development of insulin resistance (IR). WAT, which contains a very small amount of mitochondria, contributes to the formation of IR by storing triglycerides and fatty acids. WAT functions as endocrine tissue in the body, synthesizing various molecules such as leptin, ghrelin, NUCB2/nesfatin-1, and irisin along with fat storage. BAT is quite effective in energy expenditure, unlike WAT. The number of mitochondria and lipid droplets composed of multicellular cells in BAT is much higher when compared to WAT. BAT contains a protein called uncoupling protein-1 (UCP1) in the mitochondrial membranes. This protein pumps protons from the intermembrane space toward the mitochondrial matrix. When UCP1 is activated, heat dissipation occurs while ATP synthesis does not occur, because UCP1 is a division protein. At the same time, BAT regulates body temperature in infants. Its effectiveness in adults became clear after the discovery of irisin. The molecular mechanism of exercise, which increases calorie expenditure, became clear with the discovery of irisin. Thus, the isolation of irisin led to the clarification of metabolic events and fat metabolism. In this review, literature information will be given on the effect of irisin hormone on energy metabolism and metabolic syndrome (MetS)., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Hyperuricemia (HU) is a metabolic disease characterized by high uric acid levels in the blood. HU is a risk factor for diabetes, cardiovascular complications, metabolic syndrome, and chronic kidney disease. Purpose: The present study was performed to determine the effect of experimental HU on xanthine oxidase (XO), tumor necrosis factor-alpha (TNF-α), nuclear factor-kappa B (NF-κB), interleukin-17 (IL-17), cytochrome C, glutathione peroxidase (GPx), caspase-3, and 8-hydroxydeoxyguanosine (8-OHdG) levels in liver tissues of rats. Study Design: Thirty-five, male, Wistar albino-type rats were used for this study. Experimental groups were formed as follows: Group 1: control group; Group 2: potassium oxonate (PO) group; group 3: PO+NAR (naringenin; 2 weeks) group; and Group 4: PO (2 weeks)+NAR (2 weeks) group (total of 4 weeks). Methods: The first group was not given anything other than normal rat food and drinking water. In the second group, a 250 mg/kg intraperitoneal dose of PO was administered for 2 weeks. In the third group, 250 mg/kg intraperitoneal PO (application for 2 weeks) and 100 mg/kg NAR intraperitoneally 1 hr after each application were administered. In the fourth group, intraperitoneal PO administration was applied for 2 weeks, followed by intraperitoneal administration of NAR for 2 weeks (4 weeks in total). At the end of the experimental period, XO, TNF-α, NF-κB, IL-17, cytochrome C, GPx, caspase-3, and 8-OHdG levels were determined in liver tissues. Results: HU increased XO, TNF-α, NF-κB, IL-17, cytochrome C, caspase-3, and 8-OHdG levels in liver tissues. However, both 2 and 4 weeks of NAR supplementation decreased these values, and also NAR supplementation led to an increase in GPx levels in tissues. Conclusions: The results of the study show that increased inflammation, apoptosis, and DNA damage in experimental HU can be prevented by administration of NAR due to inhibition of cytochrome C, NF-κB, caspase-3, and 8-OHdG.

Alzheimer's disease (AD), especially its sporadic form (sAD), is of multifactorial nature. Brain insulin resistance and disrupted zinc homeostasis are two key aspects of AD that remain to be elucidated. Here, we investigated the effects of dietary zinc deficiency and supplementation on memory, hippocampal synaptic plasticity, and insulin signaling in intracerebroventricular streptozotocin (icv-STZ)-induced sAD in rats. The memory performance was evaluated by Morris water maze. The expression of hippocampal protein and mRNA levels of targets related to synaptic plasticity and insulin pathway was assessed by Western blot and real-time quantitative PCR. We found memory deficits in icv-STZ rats, which were fully recovered by zinc supplementation. Western blot analysis revealed that icv-STZ treatment significantly reduced hippocampal PSD95 and p-GSK3β, and zinc supplementation restored the normal protein levels. mRNA levels of BDNF, PSD95, SIRT1, GLUT4, insulin receptor, and ZnT3 were found to be reduced by icv-STZ and reestablished by zinc supplementation. Our data suggest that zinc supplementation improves cognitive deficits and rescues the decline in key molecular targets of synaptic plasticity and insulin signaling in hippocampus caused by icv-STZ induced sAD in rats., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The aim of this study was to investigate how the application of vitamin E affected the levels of chemical elements in the brain tissues of epilepsy-induced rats. The sample of 40 adult male rats was separated into 4 equal groups: Group 1: control, Group 2: vitamin E; Group 3: penicillin to promote epileptic form activity and Group 4: penicillin + vitamin E. After three months of treatment, an Atomic Absorption Spectrophotometer was used to analyze the presence of the elements in brain tissue sections (brain, brainstem, cerebellum) of the decapitated animals. The levels of magnesium in the groups that received vitamin E (G2 and 4) were significantly higher than in the control group (G1) and the first epilepsy group (G3) (p.05).Chrome and zinc levels in brain, brainstem, and cerebellum tissue of the two epilepsy groups (G3-4) decreased significantly compared to the control group (G1) and the vitamin E group (G2) (p.05). The levels of copper in the brainstem and lead in the cerebellum of the first epilepsy group (G3) were higher than in all other groups (p.05). The findings showed that the application of vitamin E in experimental epilepsy may have a limited effect on element metabolism in brain tissue. A decline in zinc levels in the brain, brainstem and cerebellum tissues in epilepsy groups constitutes another result of our study. This should be examined further to determine whether decreased levels of zinc play a role in epilepsy pathogenesis.

Objectives: This study aims to investigate the role of putrescine against brain ischemia-reperfusion (IR) injured rats administered with 250 µmol/kg exogenous putrescine and highlight the IR-associated mechanisms in energy metabolism and inflammatory pathway., Materials and Methods: The rats were divided into six groups: 1-Sham group; 2-IR group, 30 min of ischemia and 30 min of reperfusion was performed with bilateral carotid occlusion (BCAO); 3-IPR group, a single oral dose of putrescine was administered at the start of the 30-minute reperfusion; while in the other treatment groups, 4 doses of putrescine were given within 12-hour intervals. After 30 min of reperfusion, the first dose was administered immediately in the IR-PI (group 4), after 3 hr in IR-PII (group 5), and after 6 hr in IR-PIII (group 6). Interleukin-6 (IL-6), Nuclear factor NF-kappa-B (NF-kB), Adenosine triphosphate (ATP), total Nitric oxide (NO), 8-hydroxyguanosine (8-OHdG), Spermidine/Spermin N-acetyltransferase (SSAT) levels were analyzed in brain tissues., Results: IR reduced brain ATP levels; however, putrescine treatment reversed this state. Brain NO and 8-OHdG levels, and NF-kB and IL-6 levels increased significantly in the IR group and these elevations were decreased in putrescine administered groups. SSAT levels were higher in the IR-PII group. The lowest levels were observed in the IR-PIII group., Conclusion: The exogenous putrescine supplementation after cerebral IR creates neuroprotective effects independent of the time of administration; according to conditions such as formation of radicals in the brain, the spread of the inflammation and the need for consumption of energy are considered as a whole., Competing Interests: The authors declare that they do not have any conflicts of interest.

This study aimed to determine the effect of 3',4'-Dihydroxyflavonol (DiOHF) on lipid peroxidation, DNA damage and inflammation in ovarian ischaemia (I)-reperfusion (R) injury. This study was performed on 44 Wistar-albino female rats. Groups were designed as Control; Sham; I/R (the left ovary was ligated for 2 h and then reperfused for 2 h); I/R + DiOHF (after 2 h ischaemia and 2 h reperfusion, 30 mg/kg of DiOHF was given intraperitoneally and reperfusion was allowed for 2 h more); I + DiOHF + R (after 2 h I, 30 mg/kg of DiOHF was given at the beginning of 2 h reperfusion); DiOHF + I/R (2 h after DiOHF administration, the left ovary was ligated for 2 h and then reperfused for 2 h). Blood and ovarian tissue samples were analysed for GSH, MDA, 8-OHdG, SOD, and IL-6. Ovarian tissue was examined histopathologically. Ovarian I/R has led to inflammation and oxidative damage. However, DiOHF activated the antioxidant system and prevented DNA damage induced by I/R in ovarian tissue. Vascularisation, oedema, and inflammation also occurred in ovarian tissue in I/R group. The results of this study indicated that I/R led to disturbance of the oxidant/antioxidant system balance and increased DNA damage; however, DiOHF supplementation prevented DNA damage, lipid peroxidation and inflammation by increasing the antioxidant system in ovarian I/R injury in rats. However, in potential I/R situations, DiOHF application appears to be beneficial in reducing inflammation, oxidant injury, and DNA damage, and in activating the antioxidant system. IMPACT STATEMENT What is already known on this subject? Ischaemia/reperfusion (I/R) injuries lead to damage in cells or tissues due to insufficient blood flow. What do the results of this study add? Increased DNA injury and inflammatory response (IL-6) and structural impairment were treated by administration of intraperitoneal ( DiOHF) which strongly stimulated the antioxidant system, inhibited antioxidant activities, prevented DNA damage and inflammation process. What are the imp l ications of these findings for clinical practice and/or further research? This study's strength is that it is the first research demonstrates the prevention of DNA damage in ovarian I/R by DiOHF supplementation. This flavonoid (DiOHF) may be used for treatment in different ovarian ischaemia/reperfusion.

The aim of this study is to investigate how chronic running exercise affects ZIP10 levels in thymus and spleen tissue as well as immune parameters in diabetic rats. A total of 40 adult male Wistar rats were divided into 4 equal groups: group 1, control; group 2, exercise control; group 3, diabetes; group 4, diabetes + exercise. Diabetes was induced by injecting intraperitoneal streptozotocin (STZ) at a dose of 40 mg/kg twice with 24-h intervals to the animals in groups 3 and 4. The animals in group 2 and group 4 underwent exercise for 45 min on the rat treadmill for 4 weeks at 20 m/min. Twenty-four hours after the last running exercise, the animals were sacrificed under general anesthesia. Immunological parameters were determined by flow cytometric method; tissue ZIP 10 levels were determined by ELISA method. The diabetic group had the lowest natural killer (NK) and natural killer T (NKT) cells percentages. Chronic exercise partially improved NK and NKT cell percentages in diabetic rats. The diabetic group had the lowest ZIP10 levels in spleen and thymus tissue. ZIP10 values in spleen and thymus tissue of diabetes exercise group were significantly higher than diabetes group. The results of our study show that the impaired cytotoxic cell functions in diabetes are partially corrected with 4 weeks of chronic exercise, and that the suppressed ZIP 10 levels in diabetic rats are reversed by 4 weeks of chronic exercise., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Learning and memory are two of our mind's most magical abilities. Different brain regions have roles to process and store different types of memories. The hippocampus is the part of the brain responsible for receiving information and storing it in the neocortex. One of the most impressive characteristics of the hippocampus is its capacity for neurogenesis which is a process, new neurons are produced and then transformed into mature neurons and integrated into neural circuits. The neurogenesis process in the hippocampus, an example of neuroplasticity in the adult brain, is believed to aid hippocampal-dependent learning and memory. New neurons are constantly produced in the hippocampus and integrated into the pre-existing neuronal network, this allows old memories already stored in the neocortex to be removed from the hippocampus and replaced with new ones. Factors affecting neurogenesis in the hippocampus may also affect hippocampal-dependent learning and memory. The flavonoids can exert particularly powerful actions in mammalian cognition and improve hippocampaldependent learning and memory by positively affecting hippocampal neurogenesis., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The aim of this study was to determine the effect of different doses of naringenin (NAR) administration for 2 weeks in rats on brain Aquaporin-4 (AQP4), interleukin-2 (IL-2) and 8-Hydroxydeoxyguanosine (8-OhdG) levels in brain ischemia-reperfusion. Experimental groups were formed as follows; 1-Control; 2-Sham Control; 3 Ischemia/ Reperfusion (I/R); 4-Naringenin (Naringenin 50) + I/R; 5-Naringenin (naringenin 100) + I/R. I/R was performed as 1 hour occlusion of the carotid arteries (ischemia) followed by 1 hour reperfusion. Naringenin was supplied for 2 weeks by intraperitoneal. At the end of the experiment, AQP4, IL-2 and 8-OHdG levels were determined in the brain frontal cortex tissue taken from animals killed under anesthesia. AQP4, IL-2 and 8-OHdG levels increased significantly in I/R group. However, both 50 mg/kg and 100 mg/kg two-week administration of naringenin significantly decreased these increased parameters (P 0.001).The results of the study show that intraperitoneal administration of naringenin for two weeks in rats may prevent the damage caused by brain ischemia-reperfusion.

We investigated the relations among levels of metallothionein (MT); zinc (Zn) transport proteins, ZnT2, ZIP2 (ZRT and IRT-like proteins); and ZIP4, which enable Zn absorption in the small intestine of rats. We also investigated tissue Zn levels in the small intestine. We used four groups of adult male rats: group 1, control; group 2, pinealectomy (Px); group 3, Px + melatonin (MEL); group 4, MEL only. Animals in groups 3 and 4 were administered 5 mg/kg/day MEL for four weeks. At the end of the study, all animals were sacrificed and samples of duodenum, jejunum and ileum were harvested to analyze ZnT2, ZIP2, ZIP4 and MT levels using immunohistochemistry, and tissue Zn levels were measured by atomic absorption spectrophotometry. The lowest ZnT2 levels in the duodenum, jejunum and ileum, and the lowest ZIP2 levels in the duodenum and ileum were found in group 2. The lowest ZIP4 levels were found in the duodenum and jejunum, and the lowest MT levels in the duodenum and ileum were found in group 2. The highest MT values in the ileum were found in group 4. We found that ZnT2, ZIP2, ZIP4 and MT levels were reduced in the ileum compared to controls following Px, but levels approached control values after MEL administration. By its effects on ZnT2, ZIP2, ZIP4 and MT levels, MEL participates in the absorption of Zn in the rat small intestine.

Objectives: Thyroid hormones affect many enzymes, organs, and systems. They also play a role in complex biological events including development and growth. The main objective of this study was to analyze the effects of thyroid dysfunction on DNA damage and apoptosis in liver and heart tissues as well as the treatment of these disorders., Methods: Thirty-eight Wistar-albino male rats were randomly divided into five groups: 1. Control group (n=6): The rats were sacrificed without any application and liver and heart samples were collected. 2. Hypothyroidism group (n=8): Prophyltiouracil (PTU)-10 mg/kg/day was applied to induce hypothyroidism by intraperitoneal route for two weeks. 3. Hypothyroidism + Thyroxine group (n=8): After one week of PTU application (10 mg/kg/day), a high dose of l-thyroxine (1.5 mg/kg/day) was applied by intraperitoneal route for one week. 4. Hyperthyroidism group (n=8): l-thyroxine (0.3 mg/kg/day) was applied intraperitoneally to induce hyperthyroidism for two weeks. 5. Hyperthyroidism + PTU group (n=8): After one week of high dose l-thyroxine application, PTU (10 mg/kg/day) was applied for one week., Results: Liver and heart tissues were collected to evaluate 8-hydroxy-2 deoxyguanosine (8-OHdG), caspase-8 and caspase-9 levels. Hypothyroidism caused DNA damage in the liver, while hyperthyroidism caused DNA damage in the heart tissue. Hyperthyroidism also led to a significant increase in levels of caspase-8 and caspase-9 in liver tissue., Conclusions: The results of the study show that DNA damage and caspase levels in the heart and liver are affected differently in experimental hypothyroidism and hyperthyroidism., (© 2021 Walter de Gruyter GmbH, Berlin/Boston.)

This study was performed to determine the effect of zinc supplementation effects on metallothionein levels in testis ischaemia-reperfusion of rats. The experimental groups were designed as Control, Sham, Ischaemia-Reperfusion (I/R) and I/R + Zinc supplemented. Zinc supplemented as 5 mg/kg day for 3 weeks. Testis tissues were analysed for metallothionein by immunohistochemical staining procedures. Group comparison showed that the zinc-supplemented ischaemia-reperfusion group had a significantly higher level of cells strongly stained with metallothionein than all other groups. A general evaluation of the results suggests that zinc supplementation is a strong stimulant of metallothionein synthesis in the ischaemic testis tissue., (© 2021 Wiley-VCH GmbH.)

The purpose of this study was to investigate the effects of zinc and melatonin administration on interleukin-6, lipid peroxidation parameters, and element metabolism in DMBA-induced breast cancer in female rats. A total of 42 recently weaned Wistar rats were divided into 5 groups as follows: control (group 1), DMBA control (group 2), DMBA + zinc (group 3), DMBA + melatonin (group 4), and DMBA + melatonin and zinc (group 5). Malondialdehyde (MDA) and glutathione (GSH) levels in breast tissue and blood samples were determined via spectrophotometric methods. In addition, iron, magnesium, zinc, and copper levels in serum samples were determined by atomic emission, and plasma interleukin-6 levels were determined by ELISA method. The highest tissue and plasma MDA and the lowest tissue and erythrocyte GSH levels found in the study were in group 2; the highest tissue and erythrocyte GSH levels and the lowest tissue and plasma MDA levels are in group 5 (P < 0.05). Iron, magnesium, and zinc levels of groups 3, 4, and 5 were higher than the DMBA group without administration (group 2), but the copper values were significantly lower (P < 0.05). The highest IL-6 levels were determined in group 2 while IL-6 levels in the DMBA group (G5) treated with combined melatonin and zinc were lower than all other breast cancer groups (P < 0.05). According to the findings obtained in this presented study, combined zinc and melatonin therapy can contribute to the prevention of tumor growth by improving the disruption in element metabolism and suppressing IL-6 levels and reducing tissue damage that causes the cancer.

Objectives: This research was aimed to find out the effects of 3',4'-dihydroxyflavonol (DiOHF) on apoptosis, DNA damage, and tumor necrosis factor-α (TNF-α) levels in the frontal cortex of rats with induced experimental brain ischemi reperfusion., Materials and Methods: A total of 38 Wistar albino male rats were used. Groups were created as 1-Sham; 2-Ischemia-reperfusion (I/R); 3-I/R + DiOHF (10 mg/kg); 4-Ischemia + DiOHF + reperfusion; 5-DiOHF + I/R. I/R was performed by carotid artery ligation for 30 min in anesthesized animals. Following experimental applications, blood samples were taken from anesthetized rats to obtain erythrocyte and plasma. Later, the rats were killed by cervical dislocation, and frontal cortex samples were taken and stored at - 80 o C for the analysis., Results: In the ischemic frontal cortex tissue sections degenerate neuron numbers, Terminal deoxynucleotidyl transferase-dUTP nick end labeling (TUNEL) positive cell ratio and caspase-3 positive cell ratio increased. Malondialdehyde, TNF-α, and 8-OHdG levels were increased in both plasma and tissue in ischemia group, whereas tissue and erythrocyte glutathione levels were significantly suppressed. However, these values were significantly reversed by DiOHF treatment., Conclusion: The results of the study showed that I/R significantly increased apoptosis, TNF-α, and DNA damage in rats with brain I/R. However, 10 mg/kg intraperitoneal DiOHF treatment improved deterioted parameters., Competing Interests: None

Objectives: Thyroid hormones have important roles in normal development and energy regulating mechanisms as well as signaling mechanisms that affect energy consumption through central and peripheral pathways. The aim of this study was to determine the effects of thyroid dysfunction on adropin, asprosin and preptin levels in rat., Methods: The study was performed on the 38 male Wistar-albino rats. Experiment groups were designed as follows. 1-Control, 2-Hypothyroidism; To induce hypothyroidism PTU was applied by intraperitoneal as 10 mg/kg/day for 2 weeks. 3-Hypothyroidism + Thyroxine; Previously animals were made with hypothyroidism by 1 week PTU application and then 1 week l-thyroxine was given by intraperitoneal as 1.5 mg/kg/day. 4-Hyperthyroidism; Rats were made with hyperthyroidism by 3 weeks l-thyroxine (0.3 mg/kg/day). 5-Hyperthyroidism + PTU; Animals were made hyperthyroisim by l-thyroxine as groups 4, then 1 week PTU was applied to treatment of hiperthyrodism. At the end of supplementation animals were sacrificed and blood samples were collected for FT3, FT4, adropin, asprosin, preptin analysis., Results: FT3 ve FT4 levels were reduced significantly in hypothyroidism while increased in hyperthyroidism (p<0.001). Hipothyrodism led to reduces adropin, asprosin and preptin levels. And also hyperthyroidism reduced adropin and preptin levels (p<0.001)., Conclusions: The results of study show that experimental hypothyroidism and hyperthyroidism lead to significantly change to adropin, asprosin and preptin levels. However, correction of thyroid function caused to normals levels in asprosin and preptin., (© 2020 Walter de Gruyter GmbH, Berlin/Boston.)

We investigated how zinc (Zn) supplementation affects metallothionein levels in the cortex and medulla of ischemic renal tissue of rats. We used adult male rats divided into four groups: group 1, untreated control; group 2, sham-operated; group 3, ischemia-reperfusion; group 4, ischemia-reperfusion + 5 g/kg Zn. Renal tissue was analyzed using immunostaining of rat metallothionein. Cells stained with metallothionein were counted and their percentage was calculated. We found that the Zn supplemented ischemia and reperfusion group exhibited a greater percentage of cells stained strongly for metallothionein in the renal cortex than all other groups. In the renal medulla, percentages of weak staining for metallothionein in the control and ischemia and reperfusion groups were greater than those in the sham and Zn-supplemented ischemia/reperfusion groups. Our findings indicate that the main effect of Zn in the renal tissue occurs in the cortex, while metallothionein synthesis in the renal medulla is unaffected.

The inflammatory process in the human body is a physiological response involving many cellular types and mediators. It results in scar formation to separate the damaged area from the surrounding healthy tissue. Because of increased blood-brain barrier permeability following inflammation, leukocytes infiltrate the CNS and are also supplemented by proinflammatory mediators. However, an acute inflammatory process after cerebral trauma or stroke may also result in a prolonged lesion formation, leading to a severe neuronal loss. The prolonged inflammatory process in the CNS may cause serious damage to the neuronal system. It may lead to CNS damage in such a way that endangers functional integration and proinflammatory system balance. Effects of different flavonoid species on ischemia-reperfusion injury and cognition and function have also been shown in experimental studies. Flavonoids are presented broadly in plants and diets. They are believed to have various bioactive effects including anti-viral, anti-inflammatory, cardioprotective, anti-diabetic, anti-cancer, anti-aging, etc. Quercetine is the predominant dietary flavonoid. Main sources are tea, onion, and apple. It is demonstrated that the frequently consumed food like soybean, peanut, mustard, rice, sesame, olive, potatoes, onion, and oats contain flavonoids. Catechin and its derivates which are isolated from tea leaves have antioxidant activity but in low doses, their prooxidant effects are also reported. Ipriflavone which is a synthetic flavonoid may increase total calcium in bone. In this review, the effects of flavonoids species on the inflammatory process in the neurodegenerative process were examined as general., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

In the literature screening, aquaporins were found in the cerebral structures including the pia mater, choroid plexus, ependyma, piriform cortex, hippocampus, dorsal thalamus, supraoptic and suprachiasmatic nuclei, white matter and subcortical organ. Among these, the most common are AQP1, AQP4, and AQP9. The roles of aquaporins have been demonstrated in several diseases such as cerebral edema, various central nervous system tumors, Alzheimer's Disease and epilepsy. In this review, the relationship between brain/brain-injury and aquaporin, has been reviewed., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Melatonin is a neurohormone that has anticonvulsant activity in different experimental seizure models including hyperthermic febrile seizure. However, the mechanisms of this effect are not clear at the receptor level. The aim of the study was to determine which melatonin receptors involve in the hyperthermic febrile seizure model. 22-30 days Wistar male rats were used, and in children, it corresponds to 1.5-2 years. Groups were performed as (1) control, (2) ethanol/saline, (3) DMSO, (4) melatonin (MT), (5) MT + luzindole (LUZ), (6) MT + K-185, (7) MT + prazosin (PRZ), (8) MT + LUZ + K-185, (9) MT + LUZ + PRZ, (10) MT + K-185 + PRZ, and (11) MT + LUZ + PRZ + K-185. The hyperthermic febrile seizure pattern was established by keeping the rats in 45 °C hot water, and the latency, duration, and severity of seizures were determined in all groups. MT, LUZ, K-185, and PRZ were given 15, 45, 15, and 30 min before the induction of seizure, respectively. It was observed that melatonin shortened the duration of seizure, reduced the severity, and did not affect latency and that these effects were not completely blocked by receptor antagonists when compared with control, ethanol/saline, and DMSO groups. In conclusion, the fact that the anticonvulsant effect of melatonin is not completely blocked by all melatonin receptor antagonists. We can conclude that a multimodal mechanism may be responsible for the effect of melatonin receptors alone on the anticonvulsant effect of melatonin. It will be useful to design new pharmacological studies to make the subject clear.

We investigated how resveratrol affects lipid oxidation during experimental renal ischemia-reperfusion injury in rats. We used 48 adult male rats assigned to five groups: group 1, control; group 2, renal ischemia; group 3, renal ischemia + reperfusion; group 4, resveratrol + renal ischemia; group 5, resveratrol + renal ischemia + reperfusion. Plasma and renal tissue malondialdehyde (MDA), and erythrocyte and renal tissue glutathione (GSH) levels were measured and histologic changes in the renal tissue were examined. Ischemia-reperfusion affected the MDA-GSH balance adversely and caused histopathological changes in the renal tissue of the ischemia and ischemia + reperfusion groups. Resveratrol treatment normalized MDA and GSH levels as well as the histopathology that occurred in the renal tissue of the ischemia and ischemia + reperfusion groups.

This study aimed to examine the affects of 3'-4'-dihydroxyflavonol (DiOHF) on lipid peroxidation in experimental renal ischemia-reperfusion. The research was conducted on Wistar-albino type male rat. The experimental groups were formed as 1.Control; 2.Sham; 3.Ischemia; 4.Ischemia+reperfusion; 5.DiOHF+Ischemia; 6.Ischemia+ DiOHF + reperfusion. The highest tissue glutathione levels were found in groups 5 and 6. Groups 1 and 2, which were control and sham groups respectively, had the lowest tissue GSH values. Ischemia group was found to have the highest tissue malondialdehyde (MDA) level. Tissue MDA levels in group 4 were lower than those in group 3, however, higher than the levels in all other groups. Erythrocyte GSH levels in groups 5 and 6 were higher than the levels in all other groups. Group 4 has highest plasma MDA values. Plasma MDA levels in group 3 were lower than the levels in Group 4, but higher than those in other groups. The results of the study indicate that intraperitoneal DiOHF administration inhibits lipid per oxidation that intensifies in the case of renal ischemia-reperfusion injury in rats.

Resveratrol (RES) is a well-known phytocompound and food component which has antioxidative and multifunctional bioactivities. The present study aims to examine how resveratrol administration affects plasma leptin and liver glycogen levels in rats subjected to an acute swimming exercise bout. The study was carried out on Wistar-Albino type adult male rats, each group include 7 rats. Group 1, Control Group. Group 2, Control Swimming Group: The group fed on a standard diet and subjected to an acute swimming exercise bout for 30 minutes at the end of the study. Group 3, Resveratrol Group: The group fed on a standard diet and given (10 mg/kg) resveratrol in drinking water for four weeks. Group 4, Resveratrol + Swimming Group: The group fed on a standard diet, given (10 mg/kg) resveratrol in drinking water for four weeks and subjected to a 30-minute acute swimming exercise at the end of the study. Plasma leptin levels using ELISA method (ng/l) and liver glycogen levels were determined by using histochemical method (number/0.1 mm 2 ). Four weeks resveratrol administration to exercised and not-exercised rats did not cause a change in plasma leptin levels. Liver glycogen levels were 17.00 ± 3.16; 14.12 ± 2.98; 20.82 ± 1.97; 16.38 ± 1.27 (mean ± sd); respectively in groups 1, 2, 3, 4. Resveratrol administration to rats subjected to a bout of acute swimming exercise produced an effect that prevented the decrease in liver glycogen (p < 0.05). The study highlights that resveratrol supplementation may have regulatory effects on liver glycogen levels in exercised and non-exercised rats.

The present study aims to examine how resveratrol administration affects muscle glycogen levels in rats subjected to an acute swimming exercise bout. The study was conducted on adult male rats of Wistar-Albino. The 28 rats used in the study were equally divided among four groups: Group 1, Control Group: The group fed on a standard diet and not subjected to any procedure. Group 2, Control Swimming Group: The group fed on a standard diet and subjected to an acute swimming exercise bout for 30 minutes at the end of the study. Group 3, Resveratrol Group: The group fed on a standard diet and given (10 mg/kg) resveratrol in drinking water for four weeks. Group 4, Resveratrol + Swimming Group: The group fed on a standard diet, given (10 mg/kg) resveratrol in drinking water for four weeks and subjected to a 30-minute acute swimming exercise at the end of the study. At the end of the four weeks, the animals were decapitated, muscle glycogen levels using immunohistochemical method. The highest muscle glycogen levels were obtained in the resveratrol-administered Group 3 and the lowest levels in group 2 (swimming group) (p&lt;0.05). The results of the study demonstrate that resveratrol support had a protective and/or regulatory effect on mucle glycogen in both exercised and not-exercised rats.

LTP is the most intensively studied cellular model of the memory and generally divided at least two distinct phases as early and late. E-LTP requires activation of CaMKII that initiates biochemical events and trafficking of proteins, which eventually potentiate synaptic transmission, and is independent of de novo protein synthesis. In contrast, L-LTP requires gene expression and local protein synthesis regulated via TrkB receptor- and functional prions CPEB2-3-mediated translation. Maintenance of LTP for longer periods depends on constitutively active PKMζ. Throughout this review, current knowledge about early and late phases of LTP will be reviewed.

Zinc is essential in the regulation of a variety of physiological and biochemical events in the organism. It plays a critical role in maintaining the cell membrane integrity, protein-carbohydrate-lipid metabolism, immune system, wound injury and in the regulation of a number of other biological processes associated with normal growth and development. Physiological and biochemical levels of many hormones are affected by zinc metabolism. Therefore, growth impairment, hypogonadism, and some endocrine diseases are associated with the deficiency of zinc. These effects of zinc are considered versatile. Zinc increases the synthesis of the growth hormone and its number of receptors; thus, it is an important mediator in the binding of this hormone to its receptor. Found in a large quantity in the pancreas tissue, zinc has a part in the regulation of the effect of insulin. Zinc is involved to much more thyroid hormone metabolism such as hormone synthesis, receptor activity, conversion of T4 to T3, and production of carrier proteins. The low levels of zinc and high levels of leptin in obese individuals point to a critical relationship between zinc and leptin. Zinc is related to enzyme activity to melatonin synthesis. Melatonin has regulatory activity for zinc absorption from gastrointestinal system. Zinc particularly affects the conversion of testosterone to dihydrotestosterone, as 5α-reductase that is involved in this conversion is a zinc-dependent enzyme. In consideration of these relations, zinc is accepted to play critical roles in the endocrine system. The aim of the current review is to draw attention to the effects of zinc on the endocrine system.

Objective: The aim of the study was to determine the effects of zinc and melatonin supplements on the immunity parameters of female rats with breast cancer induced by DMBA., Methods: Group 1; Control, Group 2; 7,12-dimethylbenz[a]anthracene (DMBA), Group 3; DMBA + zinc, Group 4; DMBA + melatonin, Group 5; DMBA + zinc + melatonin. The rats' breast cancer was induced by DMBA 80 mg/kg. Groups 3-5 received daily 5 mg/kg doses of zinc, melatonin, and zinc + melatonin, respectively. Lymphocyte rates, T-lymphocyte subgroups, B-lymphocyte and natural killer cells (NK), and natural killer T (NKT) were evaluated., Results: The most significant increase in lymphocyte, T-lymphocyte, and CD4 lymphocyte rates was found in Group 5. The highest NKT cell rates were found in Group 3., Conclusions: Findings show that zinc and melatonin supplements have led to an increase in the immunity parameters of rats with breast cancer.

Among the trace elements, zinc is one of the most used elements in biological systems. Zinc is found in the structure of more than 2700 enzymes, including hydrolases, transferases, oxyreductases, ligases, isomerases, and lyases. Not surprisingly, it is present in almost all body cells. Preserving the stability and integrity of biological membranes and ion channels, zinc is also an intracellular regulator and provides structural support to proteins during molecular interactions. It acts as a structural element in nucleic acids or other gene-regulating proteins. Metallothioneins, the low molecular weight protein family rich in cysteine groups, are involved significantly in numerous physiological and pathological processes including particularly oxidative stress. A critical role of metallothioneins (MT) is to bind zinc with high affinity and to serve as an intracellular zinc reservoir. By releasing free intracellular zinc when needed, MTs mediate the unique physiological roles of zinc. MT expression is induced by zinc elevation, and thus, zinc homeostasis is maintained. That MT mediates the effects of zinc, besides having strong radical scavenging effects, points to the critical part it plays in oxidative stress. The present review aims to give information on metallothioneins, which have critical importance in the metabolism and molecular pathways of zinc.

Aim The present study aimed to examine the effects of melatonin supplementation on lipid peroxidation in the bone tissue of diabetic rats subjected to acute swimming exercise. Methods The study was conducted on 80 Sprague-Dawley type adult male rats which were equally allocated to eight groups: group 1, general control; group 2, melatonin-supplemented control; group 3, melatonin-supplemented diabetic control; group 4, swimming control; group 5, melatonin-supplemented swimming; group 6, melatonin-supplemented diabetic swimming; group 7, diabetic swimming; group 8, diabetic control. In order to induce diabetes, the animals were subcutaneously injected with 40 mg/kg streptozotocin (STZ). The animals were supplemented with 3 mg/kg/day melatonin intraperitoneally (IP) for 4 weeks. At the end of the study, the animals were decapitated to collect bone tissue samples which were examined to find out the malondialdehyde (MDA) (nmol/g/protein) and glutathione (GSH) (mg/dL/g protein) levels. Results The highest MDA values in the bone tissue were found in groups 7 and 8. MDA levels in the bone tissue in groups 3 and 6 were lower than the levels in groups 7 and 8, but higher than those in all other groups. Groups 3, 5 and 6 had the highest bone tissue GSH values. On the other hand, the lowest GSH level was established in groups 7 and 8. Conclusion The results of the present study indicated that the cell damage caused by acute swimming exercise and diabetes in the bone tissue could be prevented by melatonin supplementation.

Background Melatonin, an important neurohormone released from the pineal gland, is generally accepted to exercise an inhibitor effect on the thyroid gland. Zinc mediates the effects of many hormones and is found in the structure of numerous hormone receptors. Aim The present study aims to examine the effect of melatonin supplementation and pinealectomy on leptin, neuropeptide Y (NPY), melatonin and zinc levels in rats with hypothyroidism and hyperthyroidism. Methods This study was performed on the 70 male rats. Experimental animals in the study were grouped as follows: control (C); hypothyroidism (PTU); hypothyroidism + melatonin (PTU + M); hypothyroidism + pinealectomy (PTU + Pnx); hyperthyroidism (H); hyperthyroidism + melatonin (H + M) and hyperthyroidism + pinealectomy (H + Pnx). Blood samples collected at the end of 4-week procedures were analyzed to determine melatonin, leptin, NPY and zinc levels. Results It was found that thyroid parameters thyroid stimulating hormone (TSH), free triiodthyronine (FT3), free thyroxine (FT4), total T3 (TT3) and total T4 (TT4) decreased in hypothyroidism groups and increased in the groups with hyperthyroidism. The changes in these hormones remained unaffected by melatonin supplementation and pinealectomy. Melatonin levels rose in hyperthyroidism and fell in hypothyroidism. Leptin and NPY levels increased in both hypothyroidism and hyperthyroidism. Zinc levels, on the other hand, decreased in hypothyroidism and pinealectomy, but increased in hyperthyroidism. Conclusion The results of the study demonstrate that hypothyroidism and hyperthyroidism affect leptin, NPY, melatonin and zinc values in different ways in rats. However, melatonin supplementation and pinealectomy do not have any significant influence on the changes occurring in leptin, NPY and zinc levels in thyroid dysfunction.

Zinc, which is involved in the structure of all enzyme classes, is a micro nutrient element and necessary for growth and development. The ability of zinc to function without causing toxic effects is depends on the protection of its homeostasis. Zinc transporter proteins are responsible for keeping zinc at certain concentrations. Based on their predicted membrane topology, Zn transporters are divided into two major families, SLC39s/ZIPs and SLC30s/ZnTs, which transport Zn in opposite directions through cellular and intracellular membranes. ZIPs increases the zinc concentration in the cytosol. For this, the ZIPs carries the zinc from extracellular and intracellular compartments to the cytosol. ZnTs, reduces the concentration of zinc in the cytosol. For this, ZnTs carries the zinc from the cytosol to extracellular and intracellular compartments. After being transported to the cell, 50% of the zinc is found in the cytoplasm, 30-40% in the nucleus, and 10% in the plasma and organelle membranes. The expression of many zinc transporter proteins in the cell is depending on the concentration of zinc and the physiological problems. The aim of this study is to give information about association of zinc transporter proteins with physiological events and health problems.

Ischemia-reperfusion leads to damage in cell or tissue due to insufficient blood flow. The aim of present study was to determine the effect of zinc, melatonin and zinc + melatonin supplementations during 3 weeks on muscle tissue and plasma MDA and GSH levels. This study was performed on 38 male Wistar-Albino rats. Experiments groups were designed as sham-control, ischemia-reperfusion (I/R), zinc + I/R, melatonin + I/R and zinc + melatonin + I/R Ischemia-reperfusion was induced by left femoral artery occlusion (1 hour) and reopening (1 hour).  At the end of experiments tissue and blood samples were analysed for MDA and GSH. MDA levels were increased, GSH levels decreased in I/R groups. However, zinc and melatonin supplementation inhibited  MDA and increased GSH levels in I/R groups. The results of present study show that increased lipid peroxidation in muscle tissue by ischemia-reperfusion may be prevented by zinc and melatonin or zinc plus melatonin supplementation.