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目的:探讨小蘖碱(Berberine)对游离脂肪酸(free fatty acids,FFAs)诱导的小鼠肝实质细胞脂肪变性的影响。方法:胶原酶灌注分离BALB/c小鼠原代肝实质细胞并体外培养。分对照组,高脂组,高脂加小蘖碱处理组。体外测定细胞内甘油三酯的含量。利用油红染色观察细胞的脂肪样变性。通过Western印迹法检测肝实质细胞内MAPK相关信号通路磷酸化的变化。实时定量PCR检测肝实质细胞中与脂肪化密切相关的mi R-122的表达和相关靶基因的表达改变。结果:与高脂组比较,小蘖碱处理组肝实质细胞内甘油三酯含量降低,脂肪颗粒减少,脂肪变性明显改善,并具有明显的剂量效应,小蘖碱能够抑制FFAs诱导的JNK通路磷酸化。Q-PCR结果表明小蘖碱能够促进肝实质细胞内mi R-122的表达,并降低脂肪化相关基因Dgat2的表达。结论:小蘖碱能够显著改善高脂诱发的肝脂肪变性,抑制JNK通路磷酸化,其机制可能同mi R-122通路相关。
Objective: To investigate the effect of berberine on fatty degeneration of mouse hepatic parenchymal cells induced by free fatty acids (FFAs). Methods: Primary hepatic parenchymal cells of BALB / c mice were isolated by collagenase infusion and cultured in vitro. Divided into control group, high fat group, high fat plus berberine treatment group. In vitro determination of intracellular triglyceride content. The fatty degeneration of the cells was observed using oil red staining. The phosphorylation of MAPK related signal pathway in hepatic parenchymal cells was detected by Western blot. Real-time quantitative PCR was used to detect the expression of mi R-122 and related target genes in hepatic parenchymal cells. Results: Compared with the hyperlipidemia group, the content of triglyceride in hepatic parenchymal cells of berberine treatment group was decreased, the fat particle size was decreased and steatosis was significantly improved with obvious dose - effect. Berberine could inhibit FFAs - induced JNK pathway The Q-PCR results showed that berberine could promote the expression of mi R-122 and decrease the expression of Dgat2 in hepatic parenchymal cells. Conclusions: Berberine can significantly improve hepatic steatosis induced by hyperlipidemia and inhibit the phosphorylation of JNK pathway, which may be related to the mi R-122 pathway.