Berberine ameliorates lipid accumulation of mouse primary hepatocytes by decreasing fatty acids uptake
10.3969/j.issn.1001-1978.2018.03.009
- VernacularTitle:小檗碱通过抑制脂肪酸摄取降低小鼠原代肝细胞脂质沉积
- Author:
Mu-Yu YU
1
;
MIRIAYI·Alimujiang
;
Wei LIU
;
Jun YIN
Author Information
1. 上海交通大学附属第六人民医院内分泌代谢科
- Keywords:
berberine;
fatty acid uptake;
mouse pri-mary hepatocytes;
lipid accumulation;
mitochondrial respiratory chain complex I;
adenosine monophosphate-activated protein kinase
- From:
Chinese Pharmacological Bulletin
2018;34(3):337-342
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the role of berberine in mouse primary hepatocytes steatosis and whether aden-osine monophosphate-activated protein kinase(AMPK) is essential in this process in order to explore the mech-anism of non-alcoholic fatty liver disease treatment. Methods Different concentrations of oleic acid(OA) were used in mouse primary hepatocytes to determine the appropriate dose inducing steatosis. Subsequently, hepatocytes were treated with berberine and OA at the same time for 24 h serving metformin as positive con-trol. Lactic dehydrogenase (LDH) release test was performed to investigate cell viability. Lipid level was determined by oil red staining and triglyceride assay. Western blot measured the phosphorylation level of AMPK and Acetyl CoA carboxylase. An AMPK inhibi-tor compound C(CC) pre-treated hepatocytes for 1 h followed by berberine 24 h-treatment. The relationship between free fatty acid(FFA) uptake and mitochondri-al inhibition was evaluated by measuring FFA in the supernatant of OA,berberine and rotenone (mitochon-drial complex I inhibitor) group. Results Berberine could significantly reduce primary hepatocytes steatosis induced by oleic acid and stimulate AMPK and ACC phosphorylation at a non-toxic dose. In addition, CC obviously inhibited AMPK activity,but failed to dimin-ish the lipid dysregulation improvement of berberine. Berberine and rotenone intervention reduced OA up-take by 31.2% and 23.6%,respectively. Conclusion Berberine ameliorates hepatocytes lipid accumulation by suppressing fatty acid uptake,which is probably re-sulted from inhibition of mitochondrial respiratory chain complex I,independently of AMPK activation.
