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Objective This study aimed to assess the role of thiol/disulfide homeostasis and oxidative stress in the saliva of children with severe early childhood caries (S-ECC). Methods Eighty children aged 3 to 6 years were involved in this case-control study. The study consisted of two groups: the study group (S-ECC) and the control group with no caries. Thiol/disulfide homeostasis and antioxidant levels were calculated after obtaining unstimulated saliva samples from all participating children. Results The native/total thiol and total oxidant status (TOS) levels of the study group were higher than those of the control group, though not statistically significant (p > 0.05). The oxidative stress index (OSI) value was significantly higher in the study group compared to the control group (p = 0.024). Conclusion Our results confirmed that the thiol/disulfide homeostasis was reduced, and disulfide formation, which is rereducible to thiol, was insufficient in children with S-ECC to compensate oxidative stress compared with the control group. Also, thiol levels were inadequate to compensate for oxidative stress, and thiol/disulfide homeostasis was not an independent parameter for S-ECC. Besides, the increases in the TOS level and OSI value show that oxidative stress had significant effects on S-ECC's etiopathogenesis.

Abstract. This study investigates lycopene’s preventive efficacy in skeletal muscle ischemia-reperfusion (I/R) induced lung injury. Thirty-two rats were randomly assigned to control group, lycopene group, I/R group and I/R + lycopene group. In the lycopene and I/R + lycopene groups, the rats initially received 10 mg/kg/day lycopene orally for 15 days. Then, dissection around the abdominal aorta was performed in all rats under general anesthesia. The aorta was clamped at the infrarenal level in the I/R group and I/R + lycopene group for two hours before two hours of reperfusion. The mean serum levels of malondialdehyde (53.0 ± 20.14 nmol/mL) and superoxide dismutase (1.03 ± 0.16 U/mL) were higher and lower in the I/R group than the other three groups, respectively (p

Purpose: In this study, we applied platelet rich fibrin (PRF) and pure olive oil on the incision surfaces of rats. We aimed to examine whether PRF may be used safely to prevent peritoneal adhesions.Materials and Methods: Fourty rats were divided into 4 groups (n=8). Eight rats, not included in the study groups, were used to obtain PRF material. Group 1 had no surgical procedure, Group 2 was operated without medication, Group 3 was operated and received 1cc olive oil, Group 4 was operated and received 1 cc PRF. After 21 days, cecum areas were examined histopathologically. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1) and platelet-derived growth factor (PDGF) levels were measured in serum by ELISA.Results: The adhesion scores and severity of fibrosis in Group 3 and 4 were significantly lower than Group 2. Plasma TNF-α value was significantly higher in Group 2 than Group 4. Plasma PDGF value was significantly higher in Group 2 than Group 3 and 4.Discussion: PRF reduced intestinal adhesion by inhibiting the proliferation of fibroblasts and inflammatory cells, and promoting the proliferation of mesothelial cells. PRF has anti-inflammatory effect and prevented postop adhesions, based mainly on growth factors and cytokines in its content., Amaç: Bu çalışmada, adhezyon oluşması beklenen alanlara uygulanan trombositten zengin fibrin (PRF) ve saf zeytinyağının etkilerinin incelenmesi amaçlanmıştır. PRF’nin adezyona neden olup olmadığının ve PRF'nin batın içi operasyonlarda güvenle kullanıp kullanamayacağını araştırılmaktadır.Gereç ve Yöntem: Toplamda 4 grup (n=8) olmak üzere 40 adet Wistar albino rat çalışma gruplarında kullanıldı. Çalışma gruplarına dahil edilmeyen 8 rattan PRF eldesi için yararlanıldı. Grup 1’e herhangi bir cerrahi işlem yapılmadı. Adezyon modelin uygulandığı Grup 2’de ilaç kullanılmadı. Adezyon modeli sonrası Grup 3’de 1 cc zeytinyağı ve Grup 4’de 1 cc PRF uygulandı. 21 gün sonra çekum alanları histopatolojik olarak incelendi. Serumda proinflamatuar sitokinlerden tümör nekroz faktör-α (TNF-α), interlökin-6(IL-6), hücreler arası adezyon molekülü-1(ICAM-1) ve platelet-türevli büyüme faktörü(PDGF) düzeyleri ELISA yöntemiyle ölçüldü.Bulgular: Grup 3 ve 4'te adezyon skorları ve fibrozis şiddeti Grup 2'ye göre anlamlı olarak düşüktü. Plazma TNF-α değeri Grup 2'de Grup 4'e göre anlamlı olarak yüksekti. Plazma PDGF değeri Grup 2'de Grup 3 ve 4'e göre anlamlı olarak yüksekti. . Sonuç: PRF, fibroblastların ve inflamatuar hücrelerin çoğalmasını engelleyerek ve mezotelyal hücrelerin çoğalmasını teşvik ederek bağırsak yapışmasını azaltabilir. PRF, içeriğindeki büyüme faktörleri ve sitokinlere bağlı olarak antiinflamatuar etkiye sahiptir ve postop adezyonları önler.

Human adipose tissue is involved in fat storage and also plays a role in the immune response. Curcumin (CUR), a natural polyphenol is suggested to supress adipocyte differentiation in the early stage by inhibiting secretion of some regulators and the inflammatory cytokines and by activating the secretion of antiinflammatory cytokines. Our aim in this research was to examine the molecular pathways of the inhibitory effects of different doses of curcumin (0.5 µM, 5 µM, 10 µM, 20 µM, 50 µM) on the preadipocyte-adipocyte differentiation and the anti-inflammatory effect of curcumin for preventing adipocyte related oxidative and inflammatory status. Differentiation of cells was performed using Oil red O, mRNA expression levels of adiponectin, CCAAT/enhancer binding proteinα (C/EBPα), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), leptin, Nuclear Factor kappa B1 (NFκB1), peroxisome proliferator-activated receptor gamma (PPARγ), sirtuin-1 (SIRT-1), tumor necrosis factor-α (TNF-α), transient receptor potential vanilloid receptor1 (TRPV1), uncoupling protein2 (UCP2), vasculer endothelial growth factor-A (VEGF-A), vascular endothelial growth factor receptor I (VEGF-RI), VEGF-RII were evaluated in preadipocytes and adipocytes. Curcumin suppressed the differentiation of preadipocyte to adipocytes, decreased the release of proinflammatory cytokines, but it did this by regulating C/EBPα and PPARγ gene expressions outside the NF-κB pathway. Curcumin effectively suppressed adipogenic transcription factors and also adipocyte differentiation at all doses between 0.5–50 µM, but showed its anti-inflammatory effect especially in the application of curcumin of 50 µM.

Amaç: Bir kimyasal sistit hayvan modelinde intravezikal dekspantenol kullanımının mesane histolojisi ve inflamatuvar parametreler üzerindeki etkilerini klinik pratikte kullanılan kondroitin sülfat ve hyaluronik asit ile karşılaştırmak. Yöntemler: Her grupta 8 adet rat olacak şekilde 40 adet Wistar Albino rat 5 gruba ayrıldı. Bu gruplar; kontrol, kimyasal sistit (CC), CC+dekspantenol, CC+kondroitin sülfat ve CC+hyaluronik asit grupları olarak belirlendi. Deneysel sistit modeli intravezikal hidroklorik asit (0.2 mL of 0.4 NHCl) instilasyonu ile sağlandı. Kontrol grubundaki sıçanlara sadece %0.9 NaCl instilasyonu yapıldı. Tedavi gruplarından CC+dekspantenol grubuna 500 mg/kg dexpanthenol içeren 2 mL 0.9% NaCl solüsyonu,. CC+kondroitin sülfat grubuna 2 mL kondroitin sülfat (0.2%) ve CC+hyaluronik asit grubuna 2 ml hyaluronik asit(%0.5) instile edildi. Tedavi gruplarına verilen bu ajanlar dört hafta boyunca haftada iki kez uygulandı. CC ve kontrol gruplarında da benzer stres oluşturmak için aynı süre boyunca %0.9 NaCl instilasyonu yapıldı.Tedavilerin bitiminden bir gün sonra abdominal insizyon ile sistektomi yapıldı. Kalplerinden kan alındıktan sonra ratlar sakrifiye edildi. Mesane dokusu histopatolojik değişiklikler açısından incelendi. Serumda ve dokuda MDA,SOD ve prolidaz değerlerine bakıldı. Bulgular: Dokuların histopatolojik incelenmesinde dekspantenol tedavisi alan grubun lökosit sayısının sistit grubuna göre azaldığı görüldü (p0.05). Tedavi gruplarının MDA, SOD ve prolidaz değerlerindeki bu olumlu düzelme ile sistit oluşturulmayan kontrol grubundaki seviyelere yaklaştığı görüldü. Sonuç: İntertisyel sistit modelinde dekspantenolün klinikte kullanılan mevcut ajanlar gibi oksidatif stresi azaltması, anti-oksidatif etkiyi arttırması,doku düzeyindeki enflamasyonu baskılaması ve maliyetinin düşük olması nedeniyle gelecekte intertisyel sistitte tek başına yada kombine tedavide yer bulacağı kanaatindeyiz.

Amaç: Bell Paralizisi(BP) olan hastalarda Sistemik İmmun İnflamasyon İndeksi(SII), Nötrofil/Lenfosit Oranı(NLO), Platelet/Lenfosit Oranının(PLO) prognoza katkısını araştırmaktır. Materyal-Metod: BP tanısı olan 71 hasta ve kontrol grubu 40 kişi olan katılımcıların verileri retrospektif olarak değerlendirildi. Çalışma kapsamında hastaların yaşları, cinsiyetleri, BP tarafı, House-Brackmann Skorlama (HBS) sistemine göre evreleri, NLO, PLO ve SII oranları ayrıntılı olarak değerlendirildi. BP grubu, Ayrıca BP hastalarda ROC analizi yapılmış, prognostik önemi olabilecek parametreler değerlendirildi. Bulgular: Yaş ve cinsiyet dağılımı açısından gruplar uyumlu idi. BP hastalarında NLO,PLO,SII değerlerindeki yükseklik istatistiksel açıdan anlamlı idi. ROC analizinde özellikle SII parametresi prognoz açısından daha değerli bulundu. Sonuç: BP inflamatuar bir bileşeni mevcuttur. SII, NLO, PLO inflamatuar durumu gösterir ve prognostik belirteç olarak kullanılabilir.

It has been demonstrated that NT-proBNP and macrophage inhibitor cytokine-1 (MIC-1/GDF-15) are associated with cognitive functions in patients without renal disease. In the present study, we examined the association of these two molecules with cognitive functions in hemodialysis patients for the first time in the literature. A total of 94 patients were enrolled. The Mini-Mental Test and the Montreal Cognitive Assessment Test (MoCA) were applied for the purpose of measuring the cognitive functions. The NT-proBNP and MIC-1/GDF-15 levels were examined with the ELISA. The mean age of the patients was 48 ± 12; 58 (61.7%) of them were male and 21.3% were diabetic. We found that in 77% of patients have impaired cognitive functions (MoCA total score

Background: Hypertension is a major risk factor for cardiovascular diseases, stroke, congestive heart disease and renal failure. Primary hypertension is a multi-factorial complex disease and its exact etiology still remains unknown. In this study we aimed to compare serum amphiregulin and cerebellin-1 levels of primary hypertension patients with healthy subjects. Material and methods: Forty-four hypertensive patients and 44 healthy people were included. Patients with systolic blood pressure measurements ≥ 140 mm Hg and diastolic blood pressure measurements ≥ 90 mm Hg were evaluated as hypertensive. Serum amphiregulin and cerebellin 1 levels were measured using ELISA method. Results: Mean amphiregulin level was 32.1 (10.2–72.5) pg/mL in hypertension group and 36.9 (15.9–109.5) pg/mL in control group (p = 0.002). Mean cerebellin 1 levels were comparable in both groups, 82.1 (23.9–286.1) pg/mL in hypertensive group and 95.1 (60.2–293) pg/mL in control group (p = 0.261). Serum amphiregulin to predict hypertension was found to be ≤ 23 pg/mL with specificity of 97% and sensitivity of 48.5% (AUC = 0.74; 95% CI, 0.62–0.86; p = 0.001). Conclusions: Hypertension is associated with lower serum amphiregulin concentrations.

The prevalence of arrhythmia has increased in hemodialysis (HD) patients and the most frequent is atrial fibrillation (AF). It was reported that the amount of epicardial fat tissue (EFT) in the population without renal disease is closely related to AF. In the present study of ours, the relation between EFT thickness and AF was examined in HD patients. A total of 79 patients who underwent HD for periods longer than 3 months were included in the study. The mean age of the patients was 53.6 ± 15.2 years and 50.6% were male. The mean EFT thicknesses were measured as 7.2 ± 2.3 mm (3-12). A positive correlation was found between the EFT thickness and age, C-reactive protein, and left ventricle rear wall thickness. AF was found in 18 (22.8%) patients in the Holter ECG examination. When the group with AF was compared with the non-AF group; although the mean HD duration of the group with AF was longer, there were no significant differences in terms of epicardial adipose tissue thickness and other parameters. In the present study, no relations were found between EFT thickness and AF frequency in HD patients. Further studies with a larger number of the patient population are needed in this regard.

Aim:The imbalance between production of reactive oxygen species and antioxidant defense determines the degree of oxidative toxicity and severity of subsequent myocardial damage.We aimed to evaluate the anti-oxidative effects of neprilysin and angiotensin inhibition on cardiovascular target tissues in dexhamethasone-induced hypertensive rats.Methods:Thirty-six Wistar rats were divided into six groups. Three groups received 30 μg/kg/day dexamethasone for 14 days to induce arterial hypertension. Mean arterial blood pressures were verified by carotid artery cannulation. Ramipril (10 mg/kg), and sacubitril/valsartan (80 mg/kg) were administered for 18 days to the hypertensive and normotensive groups. Glutathione peroxidase, superoxide dismutase and malondialdehyde levels were evaluated in cardiovascular target tissues.Results:Serum and cardiac malondialdehyde levels were lower, while cardiac glutathione peroxidase and superoxide dismutase were higher in treatment groups than in control groups. Aortic malondialdehyde in sacubitril/valsartan group was lower; aortic and renal superoxide dismutase in sacubitril/valsartan and ramipril groups were significantly higher than in control group. Serum glutathione peroxidase was higher in hypertensive sacubitril/valsartan group than in hypertensive control group.Conclusion:We demonstrated that neprilysin and/or angiotensin inhibition had protective properties against oxidative stress exerted by dexhamethasone-induced hypertension in cardiovascular target organs, which may be mediated by reversal of natriuretic peptides degradation.m, hypertension, oxidative stress, dexamethasone, rat

Doxorubicin is an anthracycline chemotherapeutic agent that causes cardiomyopathy as a side effect. Here, we aimed to investigate the effects of linagliptin and bisoprolol on the management of doxorubicin-induced cardiomyopathy in rats. Wistar rats were divided into six groups (n = 8). Group I received saline for 4 weeks; group II received 1 mg/kg bisoprolol for 8 weeks; group III received 3 mg/kg linagliptin for 8 weeks; group IV received 1.25 mg/kg doxorubicin for 4 weeks for the induction of cardiomyopathy; group V received 1.25 mg/kg doxorubicin for 4 weeks plus 1 mg/kg bisoprolol for 8 weeks; and group VI received 1.25 mg/kg doxorubicin for 4 weeks plus 3 mg/kg linagliptin for 8 weeks. Electrocardiography and isometric mechanography were conducted to measure ventricular contractile responses. Myocardial tissue and serum samples were analyzed for oxidative and cardiotoxic markers by ELISA. Electrocardiography revealed that QRS, QT and Tp intervals were longer in group IV than group I. Doxorubicin caused a significant decrease in ventricular contraction, which was significantly prevented by bisoprolol. Doxorubicin resulted in myocardial fiber disorganization and disruption, but bisoprolol or linagliptin improved this myocardial damage. Glutathione peroxidase was significantly decreased in groups IV and V. Bisoprolol or linagliptin treatment attenuated the significant doxorubicin-mediated increase in malondialdehyde. Doxorubicin and linagliptin provided significant elevations in CK-MB activity and troponin-I levels. Doxorubicin resulted in pronounced oxidative stress. The beneficial effects of bisoprolol and linagliptin on myocardial functional, histopathological and biochemical changes could be related to the attenuation of oxidative load.

Introduction The present study evaluates the predictive value of such markers as ischemia-modified albumin (IMA), malondialdehyde (MDA) and glutathione peroxide (GSH-Px), in addition to parameters associated with inflammation, oxidative stress and ischemia, playing roles in the pathology of acute appendicitis (AA), including c-reactive protein (CRP), procalcitonin (PCT) and complete blood count (CBC) parameters and their ratios, for the diagnosis of AA in adults. Material and methods The study included 51 patients with histologically confirmed appendicitis and 45 healthy controls who referred to the emergency care unit between January and June 2018. The appendicitis cases were classified into two groups, as complicated and non-complicated, based on postoperative pathological investigations. Results Of all the appendicitis cases, 68.5% (n = 35) were non-complicated and 31.4% (n = 16) were complicated. IMA (positive LR = 3.0, negative LR = 0.1), GSH-Px (positive LR = 0.5, negative LR = 1.8), MDA (positive LR = 1.8, negative LR = 0.6), CRP (positive LR = 7.2, negative LR = 0.2), PCT (positive LR = 0.7, negative LR = 1.3), WBC (positive LR = 2.9, negative LR = 0.3), neutrophil-lymphocyte ratio (positive LR = 3.2, negative LR = 0.1) thrombocyte lymphocyte ratio (positive LR = 1.6, negative LR = 0.5) and IMA/albumin ratio (positive LR = 3.3, negative LR = 0.1) levels in the appendicitis cases were evaluated by a characteristic receiver operating characteristic (ROC) curve. In addition, IMA levels were significantly higher in the complicated cases (0.40 ± 0.05 AbsU) than in the non-complicated cases (0.29 ± 0.04 AbsU) (p Conclusion Our results showed that IMA (negative LR = 0.1), CRP (positive LR = 7.2, negative LR = 0.2), NLR (negative LR = 0.1) and IMA/albumin ratio (negative LR = 0.1) can serve as important diagnostic biomarkers for AA patients. We therefore believe that before clinically confirming an AA diagnosis, these parameters may be used as diagnostic tools in addition to CBC parameters, CRP levels and radiological imaging studies.

This study investigated the effects of curcumin and capsaicin on testicular and hepatic oxidant–antioxidant status in rats fed a high-fat diet (HFD). Male Sprague–Dawley rats were divided into 5 groups (8 rats per group). The control group was fed a normal control diet (standard laboratory chow), the HFD group was fed HFD (60% of total calories from fat), the HFD+CUR group received HFD supplemented with curcumin (1.5 g curcumin/kg HFD), the HFD+CAP group was given HFD supplemented with capsaicin (0.15 g capsaicin/kg HFD), and the HFD+CUR+CAP group received HFD supplemented with curcumin and capsaicin for 16 weeks. Hepatic and testicular thiobarbituric acid reactive substances (TBARS), reactive oxygen species (ROS), glutathione (GSH) levels, glutathione transferase activity, and Cu-Zn superoxide dismutase, glutathione peroxidase, and catalase protein expression and enzyme activities were measured. Protein expression was determined by Western blotting. GSH levels and antioxidant enzyme activities were measured with colorimetric methods. HFD slightly increased hepatic and testicular oxidative stress parameters. GSH levels did not change between groups. TBARS and ROS levels were significantly reduced in the HFD+CUR+CAP group compared with the HFD group. Liver and testis antioxidant enzyme activities and expression increased significantly with combined capsaicin and curcumin treatment. Curcumin and capsaicin treatment attenuated testicular and hepatic oxidative stress and enhanced the antioxidant defense system. The combination of capsaicin and curcumin with HFD seems to have some remarkable and beneficial effects on testicular oxidative damage in the fatty liver rat model.

Background/Aim: Anti-epileptic drugs are long-term medications; thus, side-effects are frequently seen. An important but insufficiently known side-effect is the emergence of metabolic bone diseases. The mechanism of this entity is not clearly known, but it is usually seen with the use of cytochrome P450 enzyme-inducing anti-epileptics. However, recent studies demonstrated that non-enzyme-inducing molecules also cause bone mineral impairment. The aim of this study was to shed light on the pathogenesis of anti-epileptic metabolic bone disease using bone turnover markers.Methods: This comparative, prospective case-control study included 37 patients followed-up in our outpatient clinic and 39 healthy control subjects. All the patients were female, aged over 18 years and in the premenopausal period, and had received the same anti-epileptic treatment for at least 3 months. Male patients, females who were

Background: Glomerular filtration surface area and glomerular filtration rate (GFR) are increased in patients with diabetic nephropathy, especially in the early phase of the disease. Glomerular neoangiogenesis contributes to this increased GFR. Increased GFR is associated with glomerular neoangiogenesis. Vasohibin-1 is an inhibitor of neoangiogenesis. The aim of this study is to evaluate serum vasohibin-1 levels of diabetic patients with and without diabetic nephropathy (DN). Methods: One hundred and five diabetic patients and 39 healthy controls matched for age and gender were included in the study. Diabetic patients with eGFR2 and/or those who had persistent proteinuria (>200 mg/gr) measured by urine protein/creatinine ratio (UP/C) were diagnosed as overt diabetic nephropathy (DN) if they haven’t any other known kidney diseases. Serum vasohibin-1 levels were measured by ELISA. Serum creatinine, eGFR, UP/C and vasohibin-1 levels were recorded.Results: Thirty-four percent of diabetic patients had DN. Systolic blood pressure and UP/C were higher in diabetic patients than healthy controls and age, sex, eGFR were similar. Diabetic patients have nonsignificantly lower serum vasohibin-1 levels than healthy controls. Patients with DN had higher UP/C, lower eGFR and long-standing diabetes compared to diabetic patients without nephropathy. Serum vasohibin-1 levels were similar between diabetic patients with and without DN. There was no correlation between vasohibin-1 levels and eGFR or UP/C.Conclusions: In this study for the first time we showed that diabetic patients have slightly lower vasohibin-1 levels than healthy subjects but there was no difference between diabetic patients with and without nephropathy in terms of serum vasohibin levels. Because, vasohibin-1 exhibits its anti-angiogenetic properties by acting via autocrine-paracrine pathways; local vasohibin activity at the tissue level may be more important than the circulating levels.

BACKGROUND Endothelial dysfunction (ED) is associated with high cardiovascular disease burden in hemodialysis (HD) patients. Vasohibin-1, an endothelium-derived angiogenesis inhibitor, is essential for endothelial cell survival, therefore it may be a promising marker of ED. We aimed to investigate whether vasohibin-1 levels are associated with ED markers in HD patients. METHODS Fifty HD patients and 30 healthy controls were included in the study. As markers of ED, endothelium-dependent flow-mediated dilatation (FMD), carotid intima-media thickness (CIMT), and pulse wave velocity (PWV) were examined. Serum vasohibin-1 levels were measured with ELISA. RESULTS Serum vasohibin-1 levels were low (387.7 ± 115.7 vs 450.1 ± 140.1 P = .02), FMDs' were impaired (6.65 ± 2.50 vs 10.95 ± 2.86 P

Objective: We aimed to investigate the protective effect of adrenomedullin (ADM) on cerebral tissue of rats with cerebral ischemia/reperfusion (I/R) injury. Methods: Thirty-two Wistar rats were randomized into four groups (n=8). In the I/R Group, bilateral common carotid arteries were clamped for 30 minutes and, subsequently, reperfused for 120 minutes. In the ADM Group, rats received 12 µg/kg of ADM. In the I/R+ADM Group, bilateral common carotid arteries were clamped for 30 minutes and, subsequently, the rats received 12 µg/ kg of ADM. Then, reperfusion was performed for 120 minutes. The Control Group underwent no procedure. Blood and brain tissue samples were collected for biochemical and histopathological analysis. Serum malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were analysed. Brain tissue was evaluated histopathologically and neuronal cells were counted in five different fields, at a magnification of ×400. Results: Brain MDA in I/R Group was significantly higher than in ADM Group. Brain GPx and SOD in I/R+ADM Group were significantly higher than in I/R Group. The number of neurons was decreased in I/R Group compared to the Control Group. The number of neurons in I/R+ADM Group was significantly higher than in I/R Group, and lower than in Control Group. Apoptotic changes decreased significantly in I/R+ADM Group and the cell structure was similar in morphology compared to the Control Group. Conclusion: We demonstrated the cerebral protective effect of ADM in the rat model of cerebral I/R injury after bilateral carotid artery occlusion.

BACKGROUND Acute ischemia/reperfusion (I/R) injury of skeletal muscle, an important mortality and morbidity cause, is associated with oxidative stress. Lycopene is a carotenoid pigment with potent antioxidant activity and is found in vegetables and fruits. This study aims to investigate the protective effects of lycopene against I/R injury in rat hind limb muscle model. METHODS Thirty-two Wistar-albino rats were randomly allocated to control, lycopene, I/R and I/R+lycopene groups. In lycopene and I/R+lycopene groups, the rats received 10 mg/kg/day lycopene orally for 15 days before the experiment. Dissection around abdominal aorta at the infrarenal level was performed in all rats under general anesthesia. The aorta was clamped at the infrarenal level in the I/R and I/R+lycopene groups for two hours. Then, reperfusion was allowed for two hours in these groups. Samples were obtained from the hind limb muscles of rats after sacrifice for biochemical and histopathological analyses. RESULTS Serum and tissue malondialdehyde and ischemia-modified albumin levels were significantly lower in the I/R+lycopene group compared to I/R group (p

Objective Renin angiotensinogen system (RAS) inhibitors, ramipril and sacubitril/valsartan are frequently used in the treatment of cardiovascular diseases. Although they are known as contraindicated during pregnancy in hypertensive women, there is not any outcome of their safety in male fertility after exposure to ramipril or sacubitril/valsartan. In this study, we aimed to evaluate the effects of ramipril and sacubitril/valsartan to highlight their safety in the male fertility in normotensive and hypertensive rats. Methods Adult male normotensive and dexamethasone-induced hypertensive rats were treated with sacubitril/valsartan, ramipril and saline for 18 days. Arterial blood pressures were verified using carotid artery cannulation. Male fertility parameters, including the testis weights, histopathologic scoring of the testis, sperm count, sperm motility, morphology, and serum testosterone levels, were analyzed in treated and nontreated normotensive/hypertensive rats. Results Sacubitril/valsartan or ramipril treatments did not reveal a significant difference in sperm production, testicular morphology, and radioimmunoassay of serum testosterone levels compared to the control group. However, sperm motility was significantly reduced in rats under RAS inhibition. Conclusion This finding was likely mediated by the identification of Ang receptors in the tails of rat sperm given that Ang receptors may play a role in the modulation of sperm motility. Identification of RAS-related proteins involved in sperm motility may help to explain their roles in motility. Our data provide general safety evidence for the male fertilization ability after paternal sacubitril/valsartan and ramipril exposure.

Objective Statins inhibit the 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase enzyme and thus reduce plasma cholesterol levels. Although decreased cholesterol level is the main target of anti-lipidemic drugs, cholesterol has an important role in the synthesis of lipid-based hormones such as testosterone. In this study, the alterations in serum testosterone levels were examined in rats under atorvastatin therapy and their responses to vitamin D, infliximab, and leflunomide supplementation were evaluated. Materials and methods Wistar rats were treated with atorvastatin (100 mg/kg) for 21 days to induce inhibition of the HMG-CoA reductase enzyme activity. Following statin therapy, rats received vitamin D (0.2 μg/kg/day) orally for 15 days, infliximab (7 mg/kg/day) intraperitoneally in two doses, or leflunomide (10 mg/kg/day) orally in two doses. Subsequently, the alterations in serum testosterone levels were measured by ELISA. Results Atorvastatin led to a decrease in the testosterone level compared to the vehicle group. Administration of vitamin D, infliximab, and leflunomide under HMG-CoA inhibition insignificantly increased the testosterone level compared to the atorvastatin control group. Furthermore, it appears that rats under statin administration respond better to treatment with leflunomide by achieving a greater induction in testosterone levels than with vitamin D or infliximab. Conclusion Our data provide evidence that administration of vitamin D, infliximab, and leflunomide in rats under atorvastatin treatment may ameliorate the serum testosterone levels.

üksek yağlı diyetin (YYD) neden olduğu oksidatif stresin testis fonksiyonlarını olumsuz yönde etkilediği bilinmektedir. Zerdeçal baharatının aktif bileşeni olan kurkuminin oksidan-antioksidan denge üzerine olumlu etkileri olduğu gösterilmiştir. Bu çalışmanın amacı; YYD birlikte alınan kurkuminin testiste oksidan-antioksidan denge üzerine olan etkisini incelemektir. Gereç ve Yöntem: Sprague-Dawley erkek sıçanlar dört gruba ayrılmış ve 16 hafta süreyle beslenmiştir. Birinci gruba kalorisinin %10’unun yağdan karşılandığı normal diyet, ikinci gruba kalorisinin %60’ının yağdan karşılandığı YYD, üçüncü gruba YYD’e karıştırılmış kurkumin (1g/kg yem) ve dördüncü gruba sadece normal diyet+kurkumin (1g/kg yem) verilmiştir. Deney süresi sonunda testis dokusu homojenize edilerek postmitokondriyal ve mitokondriyal fraksiyonlara ayrılmış; testiste reaktif oksijen türleri (ROS) düzeyleri florometrik yöntemle, malondialdehit (MDA) ve glutatyon (GSH) düzeyleri ile glutatyon peroksidaz (GPx), süperoksit dismütaz (SOD) ve glutatyon transferaz (GST) aktiviteleri spektrofotometrik yöntemlerle ölçülmüştür. Bulgular: YYD uygulaması, testiste postmitokondriyal ve mitokondriyal MDA düzeylerini arttırmış; sitozolik GSH düzeylerini ise azaltmıştır. YYD+Kurkumin uygulaması YYD’e bağlı artış gösteren MDA düzeylerini düşürmüş; GSH düzeyini ve GST aktivitesini ise arttırmıştır. Ancak sadece kurkumin uygulaması oksidan-antioksidan göstergeleri etkilememiştir. ROS düzeyleri ile SOD ve GPx aktiviteleri ise gruplar arasında anlamlı değişim göstermemiştir. Sonuç: Bulgularımız, YYD ile birlikte alınan kurkuminin testiküler oksidan-antioksidan dengeyi koruyucu olabileceğini göstermektedir. Ancak bu etkinin moleküler mekanizmalarının incelenmesi için ileri çalışmalar yapılması gerekmektedir., Objective: High fat diet (HFD) induced oxidative stress is known to adversely affect testicular functions. Curcumin, which is an active ingredient of turmeric spice, has been shown to reduce lipid peroxidation and stimulate cellular antioxidant enzymes. The aim of this study is to investigate the effect of dietary curcumin on the testicular oxidant-antioxidant status in rats fed on a HFD. Material and Method: Male Sprague-Dawley rats were divided into four groups. Group 1 was fed with a control diet (10% of total calories from fat). Group 2 was fed with a HFD (60% of total calories from fat). Groups 3 and 4 received a HFD and a control diet with curcumin (1g/kg diet; w/w) respectively for 16 weeks. The testis tissue was homogenized and divided into postmitochondrial and mitochondrial fractions and the reactive oxygen species (ROS) levels were measured with the fluorometric method. The malondialdehyde (MDA) and glutathione (GSH) levels and glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione transferase (GST) activities were measured with spectrophotometric methods. Results: HFD supplementation increased postmitochondrial and mitochondrial MDA levels and decreased cytosolic GSH levels in testis. MDA levels decreased with curcumin supplementation. Moreover, GSH levels and GST activity increased. However, curcumin supplementation alone did not affect oxidant-antioxidant status. ROS levels, SOD and GPx activities did not change significantly between the groups. Conclusion: Our data has shown that curcumin supplementation with HFD may prevent testicular oxidant damage. However, further studies are needed to investigate the underlying molecular mechanisms.

Abbasoglu, Semra/0000-0003-3467-9763; Oner-Iyidogan, Yildiz/0000-0001-6956-8794; Tuncdemir, Matem/0000-0002-5300-4449; KOCAK, Hikmet/0000-0003-1720-9102 WOS:000484049900002 PubMed ID: 30993920 Background. Apoptosis plays a major role in fatty liver disease. High-fat diets are related to the onset of fatty liver disease and hepatic oxidant-antioxidant imbalance. Curcumin and capsaicin are somewhat beneficial in reducing hepatic triglycerides; this is most likely because they are known to downregulate reactive oxygen species (ROS) and apoptosis. Objectives. The aim of this study was to investigate the effects of curcumin and capsaicin on apoptosis through the oxidative effect in an animal model of fatty liver disease. Material and methods. Male Sprague-Dawley rats were fed a normal control diet, a high-fat diet (HFD; 60% of total calories from fat), a HFD+curcumin (1.5 g curcumin/kg HFD), a HFD+capsaicin (0.15 g capsaicin/kg HFD), or a HFD+curcumin+capsaicin (1.5 g curcumin and 0.15 g capsaicin/kg HFD). Liver lysate levels of BAX, Bcl-2 and caspase-3 were determined via immunoblotting. Caspase-3 activity was measured with a colorimetric caspase-3 measurement kit. Total antioxidant status (TAS) and total oxidant status (TOS) were assayed using commercial kits. The generation of hepatic ROS was measured with fluorimetry. Fragmentation of DNA was detected using the TUNEL method. Results. High-fat diet caused increased expression of BAX and caspase-3, as well as increased TOS and caspase-3 activity, but decreased expression of Bcl-2. HFD+curcumin+capsaicin caused decreased BAX, caspase-3, TOS, and ROS levels as compared to HFD, but increased TAS and Bcl-2. A HFD +curcumin+capsaicin also decreased the number of TUNEL-positive cells. Conclusions. These results suggest that supplementation with curcumin and capsaicin balances the hepatic oxidant-antioxidant status and may have a protective role in the apoptotic process in an HFD-induced fatty liver model. Research Fund of Istanbul University, TurkeyIstanbul University [55331, BEK-2017-24926] This work was supported by the Research Fund of Istanbul University, Turkey, project No. 55331 and BEK-2017-24926.

Effects of curcumin (turmeric) and capsaicin (red pepper) on hepatic fat accumulation and fetuin-A expression in rats fed high-fat diet (HFD) is aimed to be investigated. Male Sprague-Dawley rats received HFD (60% of total calories from fat) and 0.15 g capsaicin/kg HFD and/or 1.5 g curcumin/kg HFD for 16 weeks. Hepatic AMPK, p-AMPK and fetuin-A expressions were determined by western blotting, liver lipid levels were measured with colorimetric methods and serum fetuin-A, insulin, leptin and adiponectin levels were detected using commercial ELISA kits. HFD increased hepatic lipid levels, fetuin-A expression and serum leptin, insülin and fetuin-A levels. Curcumin and capsaicin treatments significantly reduced hepatic fat accumulation and leptin levels; liver fetuin-A expression was decreased significantly by the curcumin treatment. Curcumin and capsaicin treatments attenuated hepatic fat accumulation and increased leptin levels related to inflammation. The suppression of hepatic fetuin-A expression is observed to be especially sensitive to curcumin.

High fat diet (HFD) is associated with oxidative stress induced fatty liver. Curcumin, an extract of Curcuma longa, has been shown to possess potent antioxidant and hypolipidemic properties. In this study, we investigated the effect of curcumin treatment on hepatic heme oxygenase-1 (HO-1) expression along with pro-oxidant–antioxidant status and lipid accumulation in rats fed an HFD. Male Sprague–Dawley rats were distributed among 4 groups: Group 1, which was fed the control diet (10% of total calories from fat); Group 2, which was fed the HFD (60% of total calories from fat); and groups 3 and 4, which received the HFD supplemented with curcumin and the control diet supplemented with curcumin (1 g/kg diet; w/w), respectively, for 16 weeks. HFD caused increases in hepatic lipid levels, production of reactive oxygen species, and lipid peroxidation. Further, HO-1 expression was significantly decreased. Histopathological examination showed hepatic fat accumulation and slight fibrotic changes. Curcumin treatment reduced hepatic lipids and oxidative stress parameters, and HO-1 expression was significantly increased. These findings suggest that increased HO-1 expression, along with suppressed oxidative stress as well as reduced hepatic fat accumulation and fibrotic changes, contribute to the beneficial effects of curcumin in attenuating the pathogenesis of fatty liver induced metabolic diseases.

The effects of curcumin on mast cell chymase activity in fatty liver and serum fetuin-A levels in rats fed a high-fat diet (HFD) were investigated. Male Sprague-Dawley rats received HFD (60% of total calories from fat) and 1 g curcumin/kg HFD for 16 weeks. Hepatic chymase activity was determined using spectrophotometric analysis while liver lipid levels were measured using colorimetric methods and serum fetuin-A, insulin, leptin, and adiponectin levels were detected using commercial enzyme-linked immunosorbent assay kits. Hepatic fat accumulation and fibrotic changes were ameliorated with curcumin treatment. Curcumin significantly reduced hepatic lipids, chymase activity, and serum fetuin-A levels. Decreased serum leptin and augmented adiponectin levels were also observed. These findings suggest that curcumin attenuated hepatic fat accumulation and regulated adipokine levels. The reduction of liver chymase activity and serum fetuin-A levels may also contribute to the beneficial effects of curcumin in fatty liver disease induced inflammatory status. Practical applications Curcumin (diferuloylmethane), which is extracted from the dried root of the rhizome Curcuma longa, is a popular dietary spice (turmeric) in Asia and used in curry. Turmeric is widely used as food component, flavoring agent, and colorant. This research revealed that dietary curcumin treatment reduces hepatic fat accumulation, ameliorates liver damage, and inflammation related to fat storage. Therefore, curcumin may be a potential protective agent in the prevention of fatty liver disease and the anti-inflammatory capacity of curcumin may reveal a beneficial application in medicine and also food technology.