异芒果苷对高脂饮食诱导大鼠肝脏损伤的改善作用

目的?探讨异芒果苷对高脂饮食诱导大鼠非酒精性脂肪肝的影响。方法?将动物随机分为4组:空白组、高脂组、异芒果苷(20、40?mg/kg)组。除空白组外，其它组动物以高脂肪饮食喂养6周，空白组给予正常饲料，从第5周起，异芒果苷组给予相应的药物治疗2周。ELISA法检测丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、甘油三酯(TG)、胆固醇(TC)、细胞因子白介素-1β(IL-1β)、白介素-6(IL-6)，肿瘤坏死因子-α(TNF-α)，采用HE染色观察肝脏病理改变，Western blot法检测肝脏Sirt1/NF-κB信号通路蛋白的表达。体外实验采用棕榈酸诱导肝脏L02细胞损伤模型，检测细胞活性以及细胞上清IL-1β、IL-6、TNF-α水平，检测细胞Sirt1/NF-κB信号通路蛋白表达。结果?体内实验结果显示，异芒果苷显著降低ALT、AST活性及TG、TC、IL-1β、IL-6、TNF-α水平（P<0.01），改善肝组织病理学改变，增加肝脏Sirt1蛋白表达（P<0.01），降低NF-κB信号通路蛋白表达（P<0.01）。体外实验结果表明，异芒果苷能显著增加L02细胞活性（P<0.01），降低细胞上清炎症因子水平（P<0.01），增加细胞Sirt蛋白表达（P<0.01），降低NF-κB信号通路蛋白表达（P<0.01）。结论?异芒果苷能显著改善高脂饮食诱导的非酒精性脂肪肝，其机制可能与调节Sirt1/NF-κB信号通路有关。 

Isomangiferin Attenuates High Fat Diet Induced Liver Injury in Rats

OBJECTIVE?To investigate the effects of isomangiferin (ISO) on high-fat diet induced nonalcoholic fatty liver disease in rats. METHODS?Animals were randomly divided into 4 groups: control group， model group which received high-fat diet， ISO group which received high-fat diet+ISO (20， 40?mg/kg). The animals were fed with a high-fat diet for six weeks. The control rats consumed a standard diet at the same time. From the fifth week， ISO group rats were treated with ISO (20，40?mg/kg) for two weeks. Alanine transaminase (ALT)， aspartate transaminase (AST)， serum triglyceride (TG)， serum cholesterol (TC) and cell supernatant cytokines (IL-1β， IL-6， TNF-α) in serum were detected. Liver pathological changes were detected by HE， and liver Sirt1/NF-κB signal pathway was detected by Western blot. In vitro cells were treated with palmitic acid to induce liver L02 cell injury model， to detect cell viability， the levels of IL-1β， IL-6 and TNF-α in cell supernatant， and Sirt1/NF-κB signaling pathway protein expression. RESULTS?The results of in vivo experiments showed that， ISO significantly reduced the levels of ALT， AST， TG， TC， serum and cell supernatant cytokines (IL-1β， IL-6， TNF-α) and improved liver histopathological changes. ISO also increased the expression of Sirt1 protein and decrease the expression of NF-κB signaling pathway protein in the liver. The results of in vitro experiments showed that ISO significantly increased L02 cell viability， reduced the level of inflammatory factors in cell supernatant， increased the expression of Sirt1 protein and decreased the expression of NF-κB signaling pathway protein in L02 cells. CONCLUSION?These results suggest that ISO is beneficial to nonalcoholic fatty liver disease via Sirt1/NF-κB pathway.