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ŞAHİN, ALİ

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ŞAHİN

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2017 - 201912020 - 20211
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Author: KARTAL ÖZER, NESRİN × Subject: NAFLD ×

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    ER stress related lipid accumulation and apoptotic cell death in nonalcoholic fatty liver diesease
    (ELSEVIER SCIENCE INC, 2017) ŞAHİN, ALİ; Demirel, Tugce; Sozen, Erdi; Sahin, Ali; Karademir, Betul; Ozer, Nesrin Kartal
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    alpha-Tocopherol supplementation reduces inflammation and apoptosis in high cholesterol mediated nonalcoholic steatohepatitis
    (WILEY, 2021) SÖZEN, AHMET ERDİ; Demirel-Yalciner, Tugce; Sozen, Erdi; Ozaltin, Esra; Sahin, Ali; Ozer, Nesrin Kartal
    Inflammation and apoptosis signaling are crucial steps in the progression from nonalcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH). Alpha-tocopherol, the most active form of vitamin E, is an important modulator of signaling mechanisms, but its involvement to cholesterol-induced NASH pathogenesis remains poorly defined. Herein we have reported a novel effect of alpha-tocopherol in the transition from hepatic steatosis to NASH. High cholesterol diet alone (without alpha-tocopherol) in rabbits elevated NASH development as indicated by increased inflammatory response, apoptotic activity and liver fibrosis. Such elevation results from induction of signaling mechanisms since the expressions of IL1 beta, phospho c-Jun/c-Jun ratio, JNK, caspase 9, CHOP and Bax were increased, and recruitment of macrophage, alpha-smooth muscle actin (alpha-SMA) and COL1A1 into the liver tissue were induced. Alpha-tocopherol supplementation inhibited inflammatory response, apoptosis and fibrosis development without affecting lipid accumulation in high cholesterol-induced NASH. Specifically, alpha-tocopherol lowered the inflammatory level as observed by reduced macrophage infiltration and JNK/c-Jun signaling. Lower inflammatory status co-occurred with the reduction of CHOP and Bax expressions as well as fibrosis-related COL1A1 and alpha-SMA levels. Taken together, alpha-tocopherol supplementation inhibits cholesterol-induced NASH development by lowering JNK/c-Jun/inflammation axis in addition to JNK/CHOP/apoptosis signaling, which might contribute to resistance against NAFLD/NASH transition.