Institute of Translational Medicine, Nanchang University, Nanchang, Jiangxi 330031, PR China.
Institute of Translational Medicine, Nanchang University, Nanchang, Jiangxi 330031, PR China.
Life Sci. 2016 Jul 15;157:131-139. doi: 10.1016/j.lfs.2016.06.001. Epub 2016 Jun 3.
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.
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.
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.
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.
二氢杨梅素（DMY）是从葡萄科蛇葡萄属显齿蛇葡萄中分离得到的一种黄酮类成分，最近有报道称其可改善非酒精性脂肪性肝病（NAFLD）患者的病情。然而，其作用机制尚不清楚。在这里，我们评估了 DMY 对 NAFLD 体外模型的影响，并研究了 DMY 治疗的信号转导途径。
以油酸（OA）诱导 L02 和 HepG2 细胞发生肝脂肪变性，建立 NAFLD 体外模型。通过流式细胞术、油红 O 染色和细胞生化测定分别评估细胞凋亡、脂质蓄积和氧化应激。通过 Western blot 和 RT-qPCR 研究参与脂质代谢的信号通路，包括 PPARγ、AMPK 和 AKT。
DMY 可防止 OA 诱导的细胞凋亡和脂质蓄积。DMY 降低了细胞内甘油三酯（TG）、胆固醇（TC）和丙二醛（MDA）的水平，同时增加了超氧化物歧化酶（SOD）的水平。DMY 抑制了 PPARγ 的表达和 AKT 的磷酸化，并促进了 AMPK 的磷酸化。
我们的研究表明，DMY 通过抑制细胞凋亡、脂质蓄积和氧化应激来改善 OA 诱导的肝脂肪变性。此外，DMY 的作用可能与其在调节 PPARγ、AMPK 和 AKT 信号通路中的作用有关。
