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    Effects of captopril and angiotensin II receptor blockers (AT1, AT2) on myocardial ischemia-reperfusion induced infarct size
    (Academic Press Ltd- Elsevier Science Ltd, 2011) Parlakpinar, Hakan; Ozer, Mehmet Kaya; Acet, Ahmet
    The renin-angiotensin system (RAS) plays a major role in regulating the cardiovascular system, and disorders of the RAS contribute largely to the cardiac pathophysiology, including myocardial ischemia-reperfusion (MI/R) injury. Two subtypes of angiotensin II (Ang II) receptors have been defined on the basis of their differential pharmacological properties. The current study was undertaken to address the question as to whether the inhibition of the angiotensin converting enzyme (ACE) by captopril and the AT(1) and AT(2) receptor blockers losartan and PD123319 modulate MI/R-induced infarct size in an in vivo rat model. To produce necrosis, a branch of the descending left coronary artery was occluded for 30 min followed by two hours of reperfusion. ECG changes, blood pressure, and heart rate were measured during the experiment. Captopril (3 mg/kg), losartan (2 mg/kg), and PD123319 (20 mu g/kg/min) were given in an IV 10 min before ischemia and were continued during the ischemic period. The infarcted area was measured by TTC staining. The volume of infarct and the risk zone was determined by planimetry. Compared to the control group (55.62 +/- 4.00%) both captopril and losartan significantly reduced the myocardial infarct size (30.50 +/- 3.26% and 37.75 +/- 4.44%), whereas neither PD123319 nor PD123319+losartan affected the infarct size volume (46.50 +/- 3.72 and 54.62 +/- 2.43). Our data indicates that captopril and losartan exert cardioprotective activity after an MI/R injury. Also, infarct size reduction by losartan was halted by a blockade of the AT(2) receptor. Therefore, the activation of AT(2) receptors may be potentially protective and appear to oppose the effects mediated by the AT(1) receptors. (C) 2011 Elsevier Ltd. All rights reserved.
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    Hepatoprotective effect of royal jelly, grape seed extract, and Lycium barbarum against diethylnitrosamine-induced liver toxicity in rats
    (2018) Bilgic, Sedat; Dogan, Zumrut; Azirak, Sebile; Erdemli, Mehmet Erman; Onderci, Muhittin; Turk, Ahmet; Ozer, Mehmet Kaya
    Aim: We aimed to investigate, the effects of royal jelly (RJ), grape seed extract (GSE), and Lycium barbarum extract (LBAE) against diethylnitrosamine (DEN) induced hepatotoxicity, in experimental animal model. Material and Methods: Fifty female Sprague Dawley rats were divided into five groups (n=10): Control, DEN, DEN+RJ, DEN+GSE, DEN+LBAE. DEN administrated groups were intraperitoneally (i.p.) injected with three separate administration of DEN (200 mg/kg), on the zero, fifteenth and thirtieth treatment day. Then 100 mg/kg of RJ was given to DEN+RJ group, 100 mg/kg of GSE was given to DEN+GSE group, and 400 mg/kg LBAE was given to DEN+LBAE group with the daily drinking water from day 0 for 16 weeks. Histopathologic alterations including apoptotic changes of liver were evaluated. Results: RJ, GSE, and LBAE treatments significantly reduced weight loss induced by DEN. DEN administrated rats significantly increases malondialdehyde (MDA) level. It also efficiently decreases glutathione (GSH) level and catalase (CAT), superoxide dismutase (SOD) activity. These results were significantly ameliorated by dietary supplements (p<0.05). In addition, they increased the total antioxidant status (TAS) level and decreased serum oxidative stress index (OSI), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma glutamyl transpeptidase (GGT) levels significantly (p<0.05). TUNEL positive cells were extremly pervasive in the livers of DEN group. Conclusion: Improvements were prominent in case of RJ > GSE > LBAE. Our results indicated that RJ, GSE and LBAE might be useful for prevention of hepatotoxicity induced by DEN via ameliorative effects on biochemical and oxidative stress indices
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    Olanzapine-induced renal damages and metabolic side effects: the protective effects of thymoquinone
    (2018) Bilgic, Sedat; Tastemir Korkmaz, Deniz; Azirak, Sebile; Guvenc, Ayse Nilay; Kocaman, Nevin; Ozer, Mehmet Kaya
    Aim: The goal of the study is to examine the protective qualities of thymoquinone (TQ) against the side-effects of olanzapine (OLZ) in an experimental model in rat kidneys. Material and Methods: Thirty five female Spraque-Dawley rats were divided into 5 groups (n=7): Control, OLZ, OLZ+TQ-1, OLZ+TQ-2, OLZ+TQ-3. All treatments were administered for two weeks by gavage. Two weeks administration of OLZ (4 mg/kg, once a day for the first week, 8 mg/kg once a day for the second week, p.o.) was given to all groups, except control. TQ was administered (25, 50, 100 mg/kg, once daily) by gastric tube. On treatment day 15, kidney tissues were removed for analysis. Results: TQ increased the total antioxidant status (TAS) and decreased creatinine (Cr), blood urea nitrogen (BUN), oxidative stress index (OSI) and total oxidant status (TOS) levels significantly (p<0.05). Conclusion: These results revealed that TQ improved the side-effects of OLZ, contributed to the oxygen radical scavenging activity, increased antioxidant activity and had ameliorative effects on recovery of increased serum biochemical and oxidative stress parameters. Thus, these results demonstrated that TQ had protective and antioxidant effects against adverse effects of OLZ in kidney of rats. TQ could be an effective course of therapy to enhance therapeutic efficacy.
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    Thymoquinone reduced RIPK1-dependent apoptosis caused by valproic acid in rat brain
    (2021) Tastemir Korkmaz, Deniz; Azirak, Sebile; Bilgic, Sedat; Bayram, Dilek; Ozer, Mehmet Kaya
    Aim: Valproic acid (VPA) is a commonly used antiepileptic drug and known to have a neurotoxic effect, but its mechanism is not yet understood. In the present study, we aimed to determine how the VPA causes cell death in the brain and to evaluate the protective effects of thymoquinone (TQ) on VPA-induced brain damage. Materials and Methods: Male Sprague–Dawley albino rats were divided into three groups: control, VPA (500 mg/kg/day) and VPA + TQ (500 mg/kg/day + 50 mg/kg/day) with seven rats in. At the end of the experiment, rats were sacrificed and brain samples were taken to measure the expression levels of Receptor-interacting serine/threonine-protein kinase-1 (RIPK1) and -3 (RIPK3) genes by quantitative real-time PCR (qRT-PCR), NADPH oxidase-4 (NOX4) and, caspase-3 (CAS-3) expression by immunohistochemistry and the structural changes in the brain tissue by histologically. Results: RIPK1 gene expression levels were significantly increased in the VPA group compared to the controls (p<0.05) and a decrease in VPA + TQ group against the VPA group. Also, NOX-4 and CAS-3 production were increased in the VPA group compared to the control group (p<0.05), and there is a markedly decrease in the VPA + TQ group compared to the VPA group. Conclusion: VPA induced RIPK1-dependent apoptosis, leading to cell deaths in the brain and TQ reduced its effects. Therefore, TQ uptake can be a supportive treatment method for long-term and high-dose VPA users to eliminate undesirable effects.