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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.