内科学
脂肪性肝炎
小檗碱
脂肪肝
医学
油红O
内分泌学
高脂血症
脂肪变性
甘油三酯
载脂蛋白E
细胞凋亡
非诺贝特
姜黄素
脂质代谢
化学
药理学
氧化应激
作者
Jin Yang,Xiao‑Jie Ma,Ling Li,Lei Wang,Ying‑Gi Chen,Jing Liu,Yan Luo,Zhen‑Jie Zhuang,Wen‑Jun Yang,Shu‑Fei Zang,Junping Shi
出处
期刊:Experimental and Therapeutic Medicine
[Spandidos Publications]
日期:2017-08-28
卷期号:14 (5): 4134-4140
被引量:18
标识
DOI:10.3892/etm.2017.5051
摘要
The aim of the present study was to explore the protective effects of Berberine (BBR) against non-alcoholic steatohepatitis (NASH). Male 4-week-old C57BL/6J Apolipoprotein E-deficient (ApoE-/-) mice were divided into the following three groups, which were given different diets: Normal chow diet (SC group); high-fat high-cholesterol diet (HFHC group); and HFHC diet supplemented with BBR (BBR group). Serum biochemical indicators of hepatic function and histological liver tissue changes were evaluated. The expression of neutrophil elastase (NE) and genes involved in the inflammatory response was measured. ApoE-/- mice fed a HFHC diet for 12 weeks developed NASH, characterized by steatosis and liver inflammation. Body weight, and serum triglyceride and cholesterol levels were markedly reduced by BBR. BBR supplementation significantly lowered serum alanine aminotransferase and aspartate aminotransferase levels in mice with HFHC diet-induced NASH, and significantly downregulated hepatic expression and activity of NE, whereas α1-antitrypsin (α1-AT) expression was significantly recovered by BBR (all P<0.05 vs. the HFHC group). Furthermore, treatment with BBR induced a significant reduction in the expression of key genes, including phospoinositide 3-kinase, nuclear factor-κB and interleukin-8, in the C-X-C chemokine receptor type 4 (CXCR4) signaling pathway (all P<0.05 vs. the HFHC group). These results suggest that BBR alleviates NASH in ApoE-/- mice fed a HFHC diet. Restoration of the balance of NE and α1-AT levels, which in turn facilitate the inhibition of the CXCR4 signaling pathways, may be involved in the hepatoprotective effect of BBR. These results indicate that BBR may be a candidate therapeutic agent for the treatment of NASH.
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