Person: AKKAN, AHMET GÖKHAN
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Publication Metadata only The Anti-Inflammatory Effects of Anacardic Acid on a TNF-alpha Induced Human Saphenous Vein Endothelial Cell Culture Model(2020-01-01T00:00:00Z) DURSUN, Erdinç; Onal, Burak; Ozen, Deniz; Demir, Bulent; Ak, Duygu Gezen; Demir, Caner; Akkan, Ahmet Gökhan; Ozyazgan, Sibel; AKKAN, AHMET GÖKHANBackground and Objective: Coronary bypass operations are commonly performed for the treatment of ischemic heart diseases. Coronary artery bypass surgery with autologous human saphenous vein maintains its importance as a commonly used therapy for advanced atherosclerosis. Vascular inflammation-related intimal hyperplasia and atherosclerotic progress have major roles in the pathogenesis of saphenous vein graft disease.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.