Dihydromyricetin ameliorates oleic acid-induced lipid accumulation in L02 and HepG2 cells by inhibiting lipogenesis and oxidative stress

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• 作者：Caifeng Xie^a ; ¹ ; Zhen Chen^a ; ¹ ; Chengfu Zhang^a ; Xin Xu^a ; Jiangbo Jin^a ; Weihua Zhan^a ; Tianyu Han^a ; Jianbin Wang^a ; ^{jianbinwang1@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Dihydromyricetin ; NAFLD ; Apoptosis ; Lipid accumulation ; Oxidative stress
• 刊名：Life Sciences
• 出版年：2016
• 出版时间：15 July 2016
• 年：2016
• 卷：157
• 期：Complete
• 页码：131-139
• 全文大小：1618 K

文摘

Dihydromyricetin (DMY), a flavonoid component isolated from Ampelopsis grossedentata, was recently reported to ameliorate nonalcoholic fatty liver disease (NAFLD) in patients. However, the underlying mechanisms of this action remain unknown. Here, we evaluate the effect of DMY on an in vitro model of NAFLD and investigate the signal transduction pathways underlying DMY treatment.

Main methods

Oleic acid (OA) induced hepatic steatosis was established in L02 and HepG2 cells as in vitro model of NAFLD. Cell apoptosis, lipid accumulation and oxide stress were evaluated by flow cytometry, oil red O staining, and cellular biochemical assays, respectively. Signaling pathways involved in lipid metabolism including PPARγ, AMPK, and AKT were investigated by Western blot and RT-qPCR.

Key findings

DMY protected cells against apoptosis and lipid accumulation induced by oleic acid. DMY decreased the levels of cellular triglycerides (TG), cholesterol (TC) and malondialdehyde (MDA), while at the same time increasing the level of superoxide dismutase (SOD). DMY suppressed the expression of PPARγ and the phosphorylation of AKT, and promoted the phosphorylation of AMPK.

Significance

Our study suggests that DMY ameliorates OA-induced hepatic steatosis by inhibiting cell apoptosis, lipid accumulation and oxide stress. Furthermore, the effect of DMY is likely associated with its role in the regulating of PPARγ, AMPK and AKT signaling pathways.