Akebia saponin D alleviates hepatic steatosis through BNip3 induced mitophagy

被引:43
作者
Gong, Li-li [1 ]
Yang, Song [1 ]
Zhang, Wen [1 ]
Han, Fei-fei [1 ]
Lv, Ya-li [1 ]
Wan, Zi-Rui [1 ]
Liu, He [1 ]
Jia, Yang-jie [1 ]
Xuan, Ling-ling [1 ]
Liu, Li-hong [1 ]
机构
[1] Capital Med Univ, Beijing Chao Yang Hosp, 8 Gongren Tiyuchang Nanlu, Beijing 100020, Peoples R China
基金
中国国家自然科学基金;
关键词
BNip3; Mitophagy; NAFLD; Akebia saponin D; FATTY LIVER-DISEASE; DIPSACUS-ASPER WALL; ASPEROSAPONIN VI; NONALCOHOLIC STEATOHEPATITIS; MYOCARDIAL-INFARCTION; AUTOPHAGY; PATHOGENESIS; DYSFUNCTION; APOPTOSIS; PATHWAY;
D O I
10.1016/j.jphs.2017.11.007
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Akebia Saponin D (ASD) is the most abundant constituent of the rhizome of Dipsacus asper Wall. The prior studies have shown that ASD alleviates hepatic steatosis targeted at the modulation of autophagy and exerts hepatoprotective effects through mitochondria. However, it is still unclear which signal transduction pathway that ASD increase autophagy and protect the mitochondria. The purpose of this paper was to explore the mechanisms through which ASD alleviates hepatic steatosis. ASD significantly reduced lipid accumulation in BRL cells. Furthermore, ASD significantly increased the mitophagy acting as increase the colocalization between mitochondria and punctate EGFP-LC3. ASD treatment increased the expression of BNip3, phospho-AMPK, prevented oleic acid (OA) induced LC3-II and phospho-mTOR expression. These effects were similar to the effects cotreatment with rapamycin. ASD treatment could not attenuate the expression of BNip3 blocked by chloroquine (CQ) or siRNA-mediated knockdown of BNip3. These results suggest that Akebia saponin D alleviates hepatic steatosis targeted at BNip3 mediated mitophagy. Activation of BNip3 via ASD may offer a new strategy for treating NAFLD. (C) 2018 The Authors. Production and hosting by Elsevier B.V.
引用
收藏
页码:189 / 195
页数:7
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