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Objective: The aim of this study was to reveal the effect of apocynin (APO) on the factors involved in obesity-related endothelial dysfunction (ED) and atherosclerosis (AS). Materials and Methods: Male Wistar albino rats were divided into control (CNT), high-fat diet (HFD) and HFD+APO groups. HFD and HFD+APO groups were fed HFD for sixteen weeks. APO (25 mg/kg) was administered to the HFD+APO group for the last four weeks. The effects of APO on: AS-related metabolic parameters (triglyceride, total cholesterol, high-density lipoprotein-cholesterol, insulin and leptin), oxidative stress (OS), [ malondialdehyde, glutathione, nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase-2, oxidised-low-density lipoprotein (ox-LDL) and 8-hydroxy-2-deoxyguanosine], low-density lipoprotein and ox-LDL uptake potential (activin receptor-like kinase-1 and lectin-like oxidized low-density lipoprotein receptor-1, respectively), tissue inflammation (myeloperoxidase, monocyte-chemoattractant-protein-1, tumor necrosis factor-alpha), ED (endothelial-nitric oxide synthase, inducible-nitric oxide synthase, nitric oxide), programmed cell death (terminal deoxynucleotidyl-transferase-dUTP-nick-end labeling, cleaved-poly-ADP-ribose-polymerase, gasdermin-D N-terminal fragment, caspase-1), smooth muscle cell transformation (alpha-smooth muscle actin), histology and ultrastructure of thoracic aorta were evaluated. Results: In obesity, APO had an ameliorative effect on metabolic parameters, OS, inflammation, ED, programmed cell death and ox-LDL uptake potential, but not on foam cell formation and LDL uptake potential. Conclusion: Apocynin may improve ED and AS in obesity by suppressing OS-linked factors involved in the early stage of AS. [ABSTRACT FROM AUTHOR]

Methotrexate (MTX) is a cytotoxic immunosuppressant that is widely used in the treatment of tumours, rheumatoid arthritis and psoriasis. This study aims to evaluate the effects of whey proteins on MTX-induced liver and kidney damage by focusing on oxidant–antioxidant systems and eating habits. The study was conducted in four groups of thirty Sprague–Dawley rats (control, control + whey protein concentrate (WPC), MTX, MTX + WPC). A single dose of 20 mg/kg MTX was administered intraperitoneally to the MTX groups. Control and MTX groups were given 2 g/kg WPC by oral gavage every day for 10 d. At the end of day 10, blood samples were drawn and liver and kidney tissues were removed. MTX administration increased the lipid peroxidation level and decreased glutathione level, superoxide dismutase and glutathione-S-transferase activities in the liver and kidney. Administration of WPC significantly reduced the damage caused by MTX in the liver and kidney. While a decrease in serum urea level and an increase in serum creatinine level were detected in the MTX group, WPC administration reversed these results up to control group levels. Administration of WPC to the MTX group significantly reversed the histopathological damage scores of the liver and kidney. WPC administration ameliorated the MTX-induced oxidative damage in the liver and kidney tissues due to its antioxidant properties. Liver and kidney damage can be prevented by using whey proteins as a nutraceutical in MTX therapy. In conclusion, whey proteins demonstrated a protective effect against MTX-induced liver and kidney damage. [ABSTRACT FROM AUTHOR]

Objectives: Nutritional obesity causes oxidant damage in the body and cataract formation in the lenses by increasing the formation of free radicals. Myrtus communis leaf extracts (Myr) have antioxidant properties, and apocynin (Apo) is an effective NADPH-oxidase inhibitor. The data on tissue boron levels are quite lacking. The aim of this novel study was to investigate the effects of Myr and Apo treatment on boron levels and oxidative lens damage in rats fed a high-fat diet (HFD). Materials and Methods: Wistar albino male rats were randomly divided into four groups: the control group, HFD group, HFD + Myr group, and HFD + Apo group. Body weight and blood lipids were determined before and after the experiment. After decapitating the rats, the lenses were removed and homogenized. Catalase (CAT) and superoxide dismutase (SOD) activities and boron, malondialdehyde (MDA), and reduced glutathione (GSH) levels in the lens homogenates were determined. Results: The HFD increased serum triglyceride (p<0.05), total cholesterol level (p<0.001), body weight (p<0.001), and lens MDA levels (p<0.01) and decreased lens GSH (p<0.05) and boron level (p<0.01), SOD (p<0.001), and CAT activity (p<0.001). However, Myr and Apo treatment reduced the rats' body weight (p<0.001), serum triglyceride (p<0.05), and total cholesterol level (p<0.001) and increased lens boron (p<0.01; p<0.001), GSH levels (p<0.05; p<0.01), and CAT activity (p<0.001). Conclusion: Both Myr and Apo may be able to reduce oxidative stress in the lenses of obese rats caused by HFD by increasing boron levels. [ABSTRACT FROM AUTHOR]

Alzheimer's disease is a challenging disease for patients due to progressive loss of cognition and behavioral disorders. Disruption of cholinergic transmission and neuroinflammation are the most important mechanisms underlying cognitive damage. Beta vulgaris L. var. cicla (BV) has been reported to have various pharmacological effects associated with its rich antioxidant content. In addition, anticholinesterase and antiinflammatory activities of BV have been demonstrated in vitro. The aim of this study is to elucidate the therapeutic effect of BV against cognitive impairment, reduction in cholinergic transmission and neuroinflammation caused by intracerebroventricular (ICV) administration of streptozotocin (STZ). STZ was administered bilaterally at a dose of 3 mg/kg via ICV to rats, and BV treatment at a dose of 2 g/kg for 21 days was administered orally to STZ-induced animals. After behavioral tests, AChE activity, TNF-α and IL-1β levels were measured in hippocampus and cortex tissues excised from decapitated animals. Novel object recognition and passive avoidance test showed that the treatment of BV reverted the ICV-STZ induced memory dysfunctions in rats. Furthermore, increased AChE levels in the hippocampal and cortical tissues of STZ-induced rats were significantly reduced with 21 days of BV treatment. In conclusion, these results confirm that STZ administration caused cholinergic hypofunction, neuronal inflammation and cognitive dysfunction in rats, and BV therapy significantly inhibited these changes with its potential neuroprotective activity. [ABSTRACT FROM AUTHOR]

Nephrolithiasis is common urological problem and stone formation has multiple underlying pathogenetic factors. We investigated the possible preventive and therapeutic effects of Urtica dioica ethanol extract (UD) on ethylene glycol-induced nephrolithiasis model in rats. Sprague-Dawley rats were divided into four groups (n = 10). The control group was given normal drinking water for 8 weeks and was administered vehicle by gastric gavage. Stone formation was induced by adding 0.75% ethylene glycol (EG) to their drinking water. UD (700 mg/kg) was given orally for 8 weeks to the preventive group and for last 4 weeks to the treatment group, respectively. At the end of the experiment, urine, blood samples and kidney tissues were obtained. In 24-hour urine samples, calcium and citrate levels were decreased and oxalate levels were increased in EG group whereas UD treatment groups reversed these parameters back to control levels. In addition, serum levels of creatinine and urea were increased in EG group, while UD significantly reduced these parameters. Malondialdehyde, 8-hydroxydeoxyguanosine and tumor necrosis alpha levels, and caspase- 3 and N-acetyl-β-glucosaminidase activities were elevated in EG group and showed a decrease in UD treated groups. Glutathione level was decreased in EG group, whereas it was increased in UD preventive group. Histological examination showed an improvement in UD treated groups. Our results suggest that UD is effective both in prevention and treatment for kidney stones. The mechanism underlying this effect may be the antioxidant effect of UD and the effect on the concentration of stone-forming components in the urine. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Urological Surgery is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: This study was designed to determine possible protective effect of betaine treatment against oxidative injury in pulmonary tissue induced with thermal trauma. METHODS: Under ether anesthesia, shaved dorsum of Wistar albino rats was exposed to a 90°C water bath for 10 seconds to induce burn injury. Betaine was administered orally (250 mg/kg) for a period of 21 days before burn injury, and single dose of betaine was administered after thermal injury. Control group rats were exposed to 25°C water bath for 10 seconds. Upon conclusion of experiment, rats were decapitated and blood was collected for analysis of pro-inflammatory cytokines and lactate dehydrogenase (LDH) activity. Lung tissue samples were taken to determine malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+K+-ATPase activity, in addition to histological analysis. RESULTS: Burn injury caused significant increase in both cytokine levels and LDH activity. In lung samples, raised MDA levels, MPO activity, and reduced GSH levels and Na+/K+-ATPase activity were found due to burn injury. CONCLUSION: Treatment of rats with betaine significantly restored GSH level and Na+K+-ATPase activity, and decreased MDA level and MPO activity. According to the findings of the present study, betaine significantly diminishes burn-induced damage in tissue. [ABSTRACT FROM AUTHOR]

Copyright of Turkish Journal of Urology is the property of Turkish Association of Urology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: The aim was to investigate the putative anti-inflammatory and anti-apoptotic effect of obestatin in a rat model of subarachnoidal haemorrhage (SAH). Methods: To induce SAH, rats were injected with 0.3 mL blood into their cisterna magna. At 48 hours rats were decapitated after neurological examination. Blood-brain barrier (BBB) permeability, brain water content, oxidative stress markers and histological analysis were done in brain tissue. Results: The results showed that neurological examination scores were increased in the SAH group and, moreover, BBB permeability was impaired and oedema formed. SAH resulted in increased levels of plasma tumour necrosis factor (TNF)- α, interleukin (IL)-1 β, IL-6 levels and caspase-3 activity. Lipid peroxidation and protein oxidation levels and myeloperoxidase activity were all increased in the brain tissue, with concomitant decreases in antioxidant enzymes. On the other hand, SAH-induced neurological impairment and oxidative brain injury were ameliorated in the obestatin-treated group. Conclusion: The present study provides the first evidence that peripheral administration of obestatin exerts potent anti-inflammatory and neuroprotective effects in SAH-induced oxidative damage by maintaining a balance in oxidant-antioxidant status through the augmentation of endogenous antioxidants and the inhibition of pro-inflammatory mediators. [ABSTRACT FROM AUTHOR]

Objectives This study aimed to investigate the antioxidant and anti-inflammatory effects of caffeic acid phenethyl ester (CAPE) on the methotrexate (MTX)-induced hepatorenal oxidative damage in rats. Methods Following a single dose of methotrexate (20 mg/kg), either vehicle (MTX group) or CAPE (10 µmol/kg, MTX + CAPE group) was administered for five days. In other rats, vehicle (control group) or CAPE was injected for five days, following a single dose of saline injection. After decapitation of the rats, trunk blood was obtained, and the liver and kidney tissues were removed for histological examination and for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and sodium potassium-adenosine triphosphatase (Na+/K+-ATPase) activity. TNF- α and IL-1 β levels were measured in the blood. Key findings Methotrexate administration increased the tissue MDA levels, MPO activity and decreased GSH levels and Na+/K+-ATPase activity, while these alterations were reversed in the CAPE-treated MTX group. Elevated TNF- α and IL-1 β levels were also reduced with CAPE treatment. Conclusions The results of this study revealed that CAPE, through its anti-inflammatory and antioxidant actions, alleviates methotrexate-induced oxidative damage, which suggests that CAPE may be of therapeutic benefit when used with methotrexate. [ABSTRACT FROM AUTHOR]

Introduction. Oxygen free radicals are involved in pathophysiology of ischemia/reperfusion (I/R) injury. This study was designed to assess the possible protective effect of pycnogenol (PYC) against I/R-induced oxidative renal damage. Materials and methods. Wistar albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 3 h of reperfusion. PYC (10 mg kg-1, i.p.) or saline was administered at 15 min prior to ischemia and immediately before the reperfusion period. At the end of the 3 h, rats were decapitated and trunk blood was collected. Creatinine, blood urea nitrogen (BUN), and lactate dehydrogenase (LDH) activity were measured in the serum samples, while proinflammatory cytokines, TNF-α, IL-1β, and IL-6 levels were assayed in plasma samples. Kidney samples were taken for the determination of tissue malondialdehyde (MDA), glutathione (GSH) levels, Na+,K+-ATPase, and myeloperoxidase (MPO) activities, and the extent of tissue injury was analyzed microscopically. Results. Ischemia/reperfusion caused a significant decrease in tissue GSH level and Na+,K+-ATPase activity, which was accompanied with significant increases in the renal MDA level and MPO activity. Similarly, serum creatinine and BUN levels, as well as LDH and IL-1β, IL-6, and TNF-α levels, were elevated in the saline-treated I/R group as compared to saline-treated control group. On the other hand, PYC treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by I/R. Conclusions. Findings of the present study suggest that pycnogenol exerts renoprotective effects, via its free radical scavenging and antioxidant activities, that appear to involve the inhibition of tissue neutrophil infiltration. [ABSTRACT FROM AUTHOR]

The correct number is: MUHDEK approval no: 81.2019.mar. Correction to: A multi-parameter evaluation of the neuroprotective and cognitive-enhancing effects of Origanum onites L. (Turkish Oregano) essential oil on scopolamine-induced amnestic rats B Correction to: Metabolic Brain Disease b https://doi.org/10.1007/s11011-022-00933-6 The published article has incorrect number of protocol approval in Ethical approval section. [Extracted from the article]

Endosulfan is a chlorinated cyclodiene insecticide which induces oxidative stress. In this study, we investigated the possible protective effect of melatonin, an antioxidant agent, against endosulfan (Endo)-induced toxicity in rats. Wistar albino rats (n = 8) were administered endosulfan (22 mg/kg/day orally) followed by either saline (Endo group) or melatonin (10 mg/kg/day, Endo + Mel group) for 5 days. In other rats, saline (control group) or melatonin (10 mg/kg/day, Mel group) was injected for 5 days, following corn oil administration (vehicle of endosulfan). Measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content were performed in liver and kidney. Furthermore, aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels, lactate dehydrogenase (LDH) activity were measured in the serum samples, while tumor necrosis factor-α (TNF-α), interleukin-β (IL-β) and total antioxidant capacity (AOC) were assayed in plasma samples. Endosulfan administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant rises in tissue MDA and collagen levels and MPO activity. Moreover, the proinflammatory mediators (TNF-α and IL-β), LDH activity, AST, ALT, creatinine and BUN levels were significantly elevated in the endosulfan-treated rats. On the other hand, melatonin treatment reversed all these biochemical alterations induced by endosulfan. Our results suggest that oxidative mechanisms play an important role in endosulfan-induced tissue damage and melatonin, by inhibiting neutrophil infiltration, balancing oxidant–antioxidant status and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury as a result of endosulfan toxicity. [ABSTRACT FROM AUTHOR]

Abstract: The present study was designed to determine the possible protective effects of Ginkgo biloba extract (EGb) against oxidative organ damage induced by irradiation (IR). Sprague–Dawley rats were exposed to whole-body IR (800cGy) after a 15-day pretreatment with either saline or EGb (50mg/kg/day), intraperitoneally, and treatments were repeated immediately after the IR. Then the rats were decapitated at either 6h or 72h after IR, where EGb or saline injections were repeated once daily. Lung, liver, kidney and ileum samples were obtained for the determination of malondialdehyde, glutathione levels, myeloperoxidase activity and collagen contents, while oxidant-induced DNA fragmentation was evaluated in the ileal tissues. All tissues were also examined microscopically and assayed for the production of reactive oxidants using chemiluminescence (CL). Lactate dehydrogenase (LDH)-an indicator of tissue damage and TNF-α were assayed in serum samples. In the saline-treated irradiation groups, glutathione levels were decreased significantly, while the malondialdehyde levels, myeloperoxidase activity and collagen content were increased in the tissues (p <0.01–0.001), which were in parallel with the increases in luminol and lucigenin CL values. In the EGb treated-IR groups, all of these oxidant responses were prevented significantly (p <0.05–0.01). LDH and TNF-α levels, which were increased significantly (p <0.01–0.001) following IR, were decreased (p <0.05–0.001) with EGb treatment. In conclusion, the present data demonstrate that EGb, through its free radical scavenging and antioxidant properties, attenuates irradiation-induced oxidative organ injury, suggesting that EGb may have a potential benefit in enhancing the success of radiotherapy. [Copyright &y& Elsevier]

Alendronate (ALD) causes serious gastrointestinal adverse effects. The aim of this study was to investigate whether taurine (TAU), a semi-essential amino acid and an antioxidant, improves the alendronate-induced gastric injury. Rats were administered 20 mg/kg ALD by gavage for 4 days, either alone or following treatment with TAU (50 mg/kg, i.p.). On the last day of treatment, following drug administration, pylorus ligation was performed and 2 h later, rats were killed and stomachs were removed. Gastric acidity and tissue ulcer index values, lipid peroxidation and glutathione (GSH) levels, myeloperoxidase (MPO) activity as well as the histologic appearance of the stomach tissues were determined. Chronic oral administration of ALD induced significant gastric damage, increasing lipid peroxidation, MPO activity and collagen content, as well as decreasing tissue GSH levels. Treatment with TAU prevented the damage and also the changes in biochemical parameters. Findings of the present study suggest that ALD induces oxidative gastric damage by a local irritant effect, and that TAU ameliorates this damage by its antioxidant and/or membrane-stabilizing effects. [ABSTRACT FROM AUTHOR]

ABSTRACT: Purpose: The role of melatonin on chronic water avoidance stress (WAS) induced degeneration of bladder epithelium (urothelium) was investigated. Materials and Methods: Wistar albino rats were exposed to WAS for 2 hours daily for 5 days (WAS group). Before exposing them to WAS 10 mg/kg melatonin (WAS plus melatonin group) was injected intraperitoneally into the animals. Bladder samples were investigated with light and electron microscopy. Lipid peroxidation and glutathione levels were also measured in the bladder. Results: In the WAS only group an increased number of mast cells in the mucosa, ulcerated areas, vacuole formation and dilated perinuclear cisternae, and dilatation in the intercellular spaces in the urothelium were observed. In the WAS plus melatonin group relatively normal urothelial topography, a decreased number of mast cells in the mucosa, some dilatation between intercellular areas, regular perinuclear cisternae and tight junctions were observed. Increased lipid peroxidation and decreased glutatione levels in WAS rats were reversed by melatonin. Conclusions: The results show that melatonin reverses WAS induced degenerative changes in the bladder. [Copyright &y& Elsevier]

Ischemia/reperfusion injury plays an important role in the pathogenesis of abdominal compartment syndrome, which is characterized by increased intra-abdominal pressure. The aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue, improves the reperfusion injury after decompression of acute abdominal hypertension. This study was carried out in Wistar albino rats. With the rats under anesthesia, an arterial catheter was inserted intraperioneally and with the use of an aneroid manometer connected to the catheter, intra-abdominal pressure was kept at 20 mm Hg (ischemia group) for 1 hour. In the ischemia/reperfusion group, pressure applied for 1 hour was decompressed and a 1-hour reperfusion period was allowed. In another ischemia/reperfusion group, octreotide was administered (50 μg/kg intraperitoneally) immediately before the decompression of intra-abdominal pressure. At the end of the experiment, liver and intestinal tissues were taken and malondialdehyde (an index of lipid peroxidation) and glutathione (a key to antioxidant) levels and myeloperoxidase (an index of tissue neutrophil infiltration) activity were estimated. The results demonstrated that tissue levels of malondialdehyde and myeloperoxidase activity were elevated, whereas glutathione levels were reduced in both the ischemia and ischemia/reperfusion groups. Octreotide treatment reversed these oxidant responses. In conclusion, increased intra-abdominal pressure causes oxidative organ damage and octreotide, by controlling the reperfusion of abdominal organs and inhibiting neutrophil infiltration, could improve the reperfusion-induced oxidative damage. Therefore its therapeutic role as a “reperfusion injury–limiting” agent must be further elucidated in intra-aortic pressure–induced abdominal organ injury. [Copyright &y& Elsevier]

Objective To investigate the effect of intravesical hyaluronic acid on Escherichia coli-induced cystitis and cystitis-induced hypercontractility in rats. Methods Bacterial cystitis was induced in Wistar female rats by intravesical inoculation of E. coli. Isotonic saline was instilled in the control group ( n = 6). The rats were either non-treated, treated with gentamycin (4 mg/kg, 5 days) or treated intravesically with hyaluronic acid (0.5 mL, 0.5%). On the eighth day, the bladder tissues were excised for histological examination, and the measurements of myeloperoxidase, superoxide dismutase and catalase activities. Contraction/relaxation responses to carbachol, isoprotrenol and papaverine were studied. Results Tissue myeloperoxidase activity was increased, but superoxide dismutase and catalase activities were decreased in bacterial cystitis, while hyaluronic acid treatment reversed these changes. In the hyaluronic acid-treated group, healing of the uroepithelium was observed, while decreased inflammatory cell infiltration was obvious in gentamycin-treated group. E. coli-induced cystitis in all rats resulted in increased contraction responses to carbachol compared with controls ( P < 0.01). Treatment with hyaluronic acid, but not gentamycin, significantly ( P < 0.05) depressed hypercontractility at maximum carbachol concentrations. In all rats with cystitis, papaverine-induced relaxation was increased, whereas isoproterenol-induced relaxation curves were not different between the studied groups. Conclusion Gentamycin treatment, despite its ameliorative effect on inflammation, had no impact on the contractile dysfunction of the injured bladder. Intravesical hyaluronic acid, in addition to its supportive role in the healing of the epithelium, seems to lower the increased threshold for contraction and to reduce oxidative stress. These findings support a potential role for hyaluronic acid in the treatment of bacterial cystitis. [ABSTRACT FROM AUTHOR]

Ulcerative colitis (UC) which has a global impact on the health care system with its recurrent and incompletely curable characteristics, affects the patients' quality of life. Gilaburu (GB; Viburnum opulus L.) is a fruit with rich polyphenol ingredient which is used ethnobotanically in Türkiye for medicinal purposes (for example, to pass kidney stones, to treat stomach, heart, and liver diseases, hemorrhages, hypertension, ulcers, common cold, tuberculosis, rheumatic and menstrual pain, and diabetes). On the other hand, the effects of GB in the experimental UC model have not been studied. This study aimed to explore the potential antioxidant and anti-inflammatory effects of GB fruit extract in improving acetic acid (AA)-induced UC. Starting immediately after (AA + GB group) or 1 week before (GB + AA + GB group) the colitis induced by intrarectal AA (5%; v/v) administration, the rats orally received GB (100 mg/kg) once per day for 3 days. The control and AA groups were administered orally saline (1 ml), while the AA + SS group were administered sulfasalazine (SS; 100 mg/kg; orally) as a positive control once per day for 3 days. Distal colonic tissue specimens were obtained for the histological and biochemical [myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), chemiluminescence (CL), caspase-3, 8-hydroxy-2'-deoxyguanosine (8-OHdG), matrix metalloproteinase (MMP)-9, transforming growth factor (TGF)-β 1 , smad-3 and cytokine (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-8, interferon (IFN)-γ), measurements] evaluations on the 3rd day. Elevated macroscopic and microscopic damage scores, high tissue wet weight values, increased tissue-associated MPO, MDA, CL, caspase-3, 8-OHdG, cytokines (TNF-α, IL-1β, IL-6, IL-8), MMP-9, TGF-β 1 , smad-3 levels, and decreased GSH values of the AA group were all reversed by GB treatments (AA + GB and GB + AA + GB groups) (p < 0.05–0.001). However, sulfasalazine treatment (AA + SS group) did not change the IL-8, 8-OHdG, MMP-9, and TGF-β 1 measurements significantly. Gilaburu shows both anti-inflammatory and antioxidant effects against AA-induced colonic damage by suppressing neutrophil infiltration, regulating inflammatory mediators, inhibiting reactive species production, lipid peroxidation, and apoptosis, conserving endogenous antioxidant glutathione, and ameliorating oxidative DNA damage. Since the current ulcerative colitis drugs display limited benefits and adverse side effects, potential therapeutic and/or prophylactic role of gilaburu can be evaluated in ulcerative colitis. [Display omitted] • Gilaburu (GB) suppresses neutrophil infiltration to the inflamed colonic tissue. • GB prevents lipid peroxidation and endogenous antioxidant glutathione depletion. • GB reduces toxic oxygen and nitrogen metabolites in the acetic acid-induced colitis. • GB improves oxidative DNA damage and inhibits apoptosis in tissues of colitic rats. • GB exerts anti-inflammatory activity by reducing/inhibiting proinflammatory cytokines. [ABSTRACT FROM AUTHOR]

Abstract: Background: Despite recent advances, severe burn is one of the most common problems faced in the emergency room. Major thermal injury induces the activation of an inflammatory cascade resulting in local tissue damage, to contribute to the development of subsequent damage of multiple organs distant from the original burn wound. Objective: Silymarin, the major component of milk thistle has been shown to have antioxidant properties. In the present study, we investigated the putative antioxidant effect of local or systemic silymarin treatment on burn-induced oxidative tissue injury. Methods: Wistar albino rats were exposed to 90°C bath for 10s to induce burn. Silymarin either locally (30mg/kg) applied on 4cm2 area or locally+systemically (50mg/kg, p.o.) was administered after the burn and repeated twice daily. Rats were decapitated 48h after injury and blood was collected for tumor necrosis factor-α (TNF-α) and lactate dehydrogenase (LDH) activity. In skin tissue samples malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and luminol-lucigenin chemiluminescense (CL) were measured in addition to the histological evaluation. Results: Burn caused a significant increase in TNF-α and LDH levels. MDA levels were increased and GSH levels were decreased in the skin at 48h after-burn. Both local and systemic silymarin treatments significantly reversed these parameters. The raised MPO activity and luminol-lucigenin CL were also significantly decreased. Conclusion: Results indicate that both systemic and local administration of silymarin was effective against burn-induced oxidative damage and morphological alterations in rat skin. Therefore, silymarin merits consideration as a therapeutic agent in the treatment of burns. [Copyright &y& Elsevier]

Summary: We studied the potential effects of taurine, a free radical scavenger, on chronic water avoidance stress (WAS)-induced degeneration of the mucosa of the urinary bladder in experimental rats. Wistar albino rats were exposed to WAS for 2h/day, for 5 days (WAS group). Before exposing them to WAS, taurine (50mg/kg) (WAS+taurine group) was injected intraperitonally into the animals. Samples of urinary bladder were then investigated by light and scanning electron microscopy. Lipid peroxidation and gluthathione levels were also measured in the urinary bladder. In the WAS-only group, inflammatory cell infiltration, increased number of mast cells in the mucosa and ulcerated areas were observed. In the WAS+taurine group, relatively normal urothelial topography with microvilli, moderate inflammatory cell infiltration and decreased numbers of mast cells in the mucosa were observed. The increased lipid peroxidation and decreased glutathione levels in WAS rats were reversed by taurine treatment. We conclude that taurine protects against WAS-induced oxidant urinary bladder injury, and thus may be a possible therapeutic agent against interstitial cystitis, the symptoms of which are aggravated by stress conditions. [Copyright &y& Elsevier]