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目的:研究高脂饮食肝损伤中结构型(cNOS)、诱导型(iNOS)一氧化氮(NO)合成酶及凋亡相关基因Bax、Bcl-2表达的变化,在进一步探讨脂肪性肝损伤机制的同时观察黄连素的干预调控作用。方法:建立高脂饮食大鼠肝损伤模型,ig给予黄连素20,40,60 mg·kg-1,测定血中TC,TG,HDL,LDL含量及ALT,GST活性和肝中NO含量;免疫组化方法观察cNOS,iN- OS,Bax,Bcl-2的表达。结果:黄连素可使血中TC,TG,LDL含量及sALT,sGST活性下降,呈良好的剂量依赖关系,对HDL无明显作用;能显著抑制肝组织中NO的生成;黄连素对高脂饮食大鼠肝组织中iNOS,Bax表达有一定的抑制作用,但作用无显著性差异;可显著上调肝组织中cNOS及Bcl-2的表达,但不呈剂量依赖关系。结论:黄连素可保护南脂饮食所致的肝损伤,可显著上调抗凋亡基因Bcl-2的表达,提示黄连素可能通过抗肝细胞凋亡保护高脂饮食引起的肝细胞损伤。
Objective: To study the changes of cNOS, inducible nitric oxide (NO) synthase and apoptosis-related genes Bax and Bcl-2 in liver injury induced by high-fat diet, and further explore the mechanism of fatty liver injury. At the same time, observe the interference and regulation of berberine. METHODS: A rat model of liver injury induced by high-fat diet was established. The berberine levels were 20, 40 and 60 mg·kg-1. The contents of TC, TG, HDL, LDL, ALT, GST activity and NO in liver were determined. The expression of cNOS, iN-OS, Bax and Bcl-2 were observed by histochemical method. RESULTS: Berberine could decrease the content of TC, TG, LDL, sALT and sGST in blood, showed a good dose-dependent relationship, had no significant effect on HDL, and could significantly inhibit the production of NO in liver tissue; berberine on high-fat diet The expression of iNOS and Bax in liver tissue of rats was inhibited, but there was no significant difference. The expression of cNOS and Bcl-2 in hepatic tissue was significantly up-regulated, but there was no dose-dependent relationship. Conclusion: Berberine can protect the liver injury caused by Nanzhi diet, and can significantly up-regulate the expression of anti-apoptosis gene Bcl-2, suggesting that berberine may protect hepatocyte damage caused by high-fat diet through anti-hepatocyte apoptosis.