姜黄素对大鼠非酒精性脂肪性肝病的治疗作用及其对肝脏瘦素表达的影响

Therapeutic effect of curcumin on nonalcoholic fatty liver disease in rats and its influence on the expression of leptin in liver

目的研究姜黄素对大鼠非酒精性脂肪性肝病(NAFLD)的治疗作用以及对肝脏瘦素表达的影响。方法采用高脂诱导大鼠NAFLD模型,设立正常对照组、NAFLD模型组及3种不同浓度的姜黄素治疗组。称量各组大鼠体重/肝湿重,计算肝指数;检测各组大鼠血清甘油三酯(TG)和总胆固醇(TC)含量;采用HE染色对各组大鼠肝组织进行病理学检测;采用免疫组织化学法对各组大鼠肝组织瘦素蛋白进行检测;采用PCR法对各组大鼠肝组织瘦素m RNA进行检测。结果与NAFLD模型组相比,治疗组大鼠肝指数及血清中TG、TC含量均降低,肝组织脂肪变性程度明显减轻。与正常组比较,模型组大鼠肝组织瘦素m RNA及蛋白的表达水平明显升高(P<0.05)。与模型组比较,治疗组大鼠肝组织瘦素m RNA及蛋白的表达含量明显减少(P<0.05),瘦素m RNA及蛋白的表达水平以高浓度治疗组降低更加明显(P<0.01)。结论姜黄素可减轻高脂诱导的NAFLD大鼠肝组织的脂肪变性,其机制可能与姜黄素抑制肝组织瘦素的表达有关。

Objective To study the therapeutic effect of curcumin on nonalcoholic fatty liver disease （NAFLD） in rats and its influence on the expression ofleptin in liver. Methods We used high fat diet induced NAFLD model in rats, and established normal control group, NAFLD model group and three treatment groups with different concentrations of curcumin. The liver indexes were calculated by weighing the body masses and the liver masses of the rats in each group. We detected the triglyceride （TG） and total cholesterol （TC） in the serum of rats by biochemical methods. Pathological changes of the liver tissues were detected by HE staining. We detected the leptin protein and mRNA in liver tissues of rats by immunohistochemical method and PCR method respectively. Results Compared with the NAFLD model group, the liver indexes and the contents of TC and TG were decreased in the different treatment groups, and fatty degeneration of the liver tissue was significantly reduced. Compared with the normal control group, the expression levels ofleptin mRNA and protein were significantly higher in the NAFLD model group （P〈0.05）. Compared with the NAFLD model group, the expression levels of leptin mRNA and protein were significantly reduced in the liver tissue of the different treatment groups （P〈0.05）, while the expression levels of leptin mRNA and protein were lowest in the treatment group with high dose curcumin （P〈0.01）. Conclusion Curcumin can reduce the fatty degeneration of liver tissue of NAFLD induced by high fat diet and its mechanism may be related to the inhibition of expression of leptin in the liver tissue.