Person: AKKAN, AHMET GÖKHAN
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Publication Metadata only Effect of Three PDEIs on Neuroprotective and Autophagy Proteins in vitro AD Model(2021-01-01T00:00:00Z) Saygisever-Faikoglu, Kubra; Faikoglu, Gokhan; Celik, Hande; Ugur, Sedat Askin; AKKAN, Ahmet Gökhan; Kelicen-Ugur, Pelin; Ozyazgan, Sibel; AKKAN, AHMET GÖKHANBackground and Objective: The effects of PDEIs on neuroprotective SIRT1 and SESN2, on the autophagy-related proteins, are unknown but neuroprotective enzymes (sirtuins and sestrins) with autophagy genes are involved in the pathogenesis of Alzheimer-s disease. In this study, we aimed to elucidate the effect of three PDE Inhibitors (PDEIs) as autophagy enhancers and provide insights into their neuroprotective effects. Materials and Methods: HT-22 cells were exposed to A$ 25-35 with or without PDEIs for 32 hrs. qRT-PCR was performed for SIRT1, SESN2, ATG5 and BECN1 genes. Western blot analysis was performed for neuroprotective SIRT1, SESN2 proteins and autophagy proteins such as p-mTOR/mTOR, p-AMPK/AMPK and LC3. Results: A$ 25-35 exposure decreased SIRT1, ATG5 and BECN1 expression, while PDEIs prevented these genes from the A$ 25-35 induced decrease. Increased SESN2 gene expression by A$ 25-35 exposure was decreased by PDEIs treatment. Western blot experiment has also shown that SIRT1, p-AMPK and autophagy marker LC3II were decreased, whereas SESN2 and p-mTOR were elevated in the A$ 25-35 exposed HT-22 cells. Co administration of three PDEIs with A$ 25-35 recovered SIRT1, p-AMPK and LC3II decline and compensated SESN2 increase by elevating SIRT1, p-AMPK and LC3II expression and decreasing p-mTOR expression. Conclusion: The present study revealed the significant neuroprotective and autophagy stimulating potential of three PDEIs in A$-induced in vitro AD model. SIRT1 is a novel candidate for determining new, safe and effective treatment strategies and PDEI-mediated SIRT1 increase may advocate autophagy activation through different autophagy components.Publication Metadata only Investigation of the pharmacological potential of myricetin on alcohol addiction in mice(2022-01-01T00:00:00Z) Yunusoglu, Oruc; BUKHARI, ANDLEEB; Turel, Canan Akunal; Demirkol, Muhammed Hamdi; Berköz, Mehmet; AKKAN, Ahmet Gökhan; AKKAN, AHMET GÖKHANAlcohol addiction is one of the leading causes which is associated with morbidity and mortality with outcomes in high healthcare and economic costs. Myricetin is a flavonoid that demonstrates therapeutic actions in many central nervous system diseases. In the current study, the conditioned place preference (CPP) tests were performed W examine the effects of myricetin on ethanol reward. During conditioning, intraperitoneal (i.p) administration of ethanol (2 g/kg) and serum physiologic were given on alternate days for 8 days. In order to evaluate the effect of myricetin on the development of alcohol addiction, myricetin was injected into mice 30 minutes before ethanol administration. Subsequently, a daily myricetin injection was performed to evaluate the effect of myricetin on the extinction of alcohol addiction. Finally, ethanol was administered 900 seconds after different dose myricetin administration, and reinstatement was evaluated immediately thereafter. Systemic ethanol (2 g/kg, i.p) administration significantly produced CPP. Myricetin (5 and 10 mg/kg, i.p) attenuated the development of ethanol addiction (p < 0.05). Systemic myricetin injections immediately after each extinction period precipitated extinction and decreased reinstatement (10 mg/kg, i.p, p < 0.05, respectively). Ethanol alone and in combination with myricetin did not change locomotor activity and motor coordination. As a result, it can be suggested that myricetin is effective in attenuating the rewarding effect of alcohol in mice and can be used for the adjunctive therapy for alcohol addiction. In addition, it will be appropriate to conduct mechanistic experimental studies regarding these results in the future.