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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Sheng-Jiang Powder Ameliorates High Fat Diet Induced Nonalcoholic Fatty Liver Disease via Inhibiting Activation of Akt/mTOR/S6 Pathway in Rats
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Sheng-Jiang Powder Ameliorates High Fat Diet Induced Nonalcoholic Fatty Liver Disease via Inhibiting Activation of Akt/mTOR/S6 Pathway in Rats

机译：生姜散通过抑制大鼠Akt / mTOR / S6途径的活化来减轻高脂饮食诱导的非酒精性脂肪肝疾病

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Background and Aims. Nonalcoholic fatty liver disease (NAFLD) is an alarming public health problem that directly contributes to increased prevalence of liver cirrhosis and hepatic cell cancer, but without any specific pharmacological option. Sheng-jiang powder (SJP), an empirical Chinese medicine formula to treat NAFLD, showed great efficacy but the specific mechanisms have never been reported. Therefore, we performed this study to explore the effect of SJP on NAFLD and the potential mechanism. Methods. NAFLD was induced by high fat diet (HFD) feeding. Rats were treated with SJPormal saline daily for 10 weeks and all rats were euthanized after 12 weeks’ feeding. Liver tissue samples were obtained for biochemistry test and pathological evaluation. Additionally, oleic acid induced LO2 cells were employed to simulate a cell model of NAFLD. Cells were subjected to western blotting for Akt, mTOR, S6, SREBP1-c, and FASN detection after coincubated with SJP, LY294002 (a selective PI3K inhibitor), or the combination for 24h. Results. HFD significantly induced hepatic steatosis. Plenty of lipid droplets were observed under transmission electron microscope. The ultrastructure of liver cells showed distinct changes with obvious endoplasmic reticulum expansion, mitochondrial contraction, and cell matrix solidification. Although no difference was detected in serum hepatic enzymes and tissue proinflammatory cytokines, the tissue level of SOD and GSH-px was much lower and the pathologic injuries were much severe in HFD feeding rats. However, SJP treatment significantly attenuated the ultrastructure changes and protected rat liver against inflammatory injury. Abundant of lipid droplets and high expression of pAkt, pmTOR, pS6, and FASN were observed in oleic acid treated LO2 cells, while these changes were restored by SJP treatment. Conclusions. SJP is efficient in attenuating HFD induced NAFLD in rats and this effect might be partly related to the inhibition of Akt/mTOR/S6 pathway.
机译：背景和目标。非酒精性脂肪肝疾病（NAFLD）是一个令人震惊的公共卫生问题，直接导致肝硬化和肝细胞癌的患病率上升，但没有任何特定的药理选择。盛江散（SJP）是一种治疗NAFLD的经验性中药配方，具有很好的疗效，但具体机制尚未见报道。因此，我们进行了这项研究，以探讨SJP对NAFLD的影响及其潜在机制。方法。 NAFLD是由高脂饮食（HFD）喂养引起的。每天用SJP /生理盐水治疗大鼠10周，喂食12周后将所有大鼠安乐死。获得肝组织样品用于生化测试和病理评估。另外，使用油酸诱导的LO2细胞来模拟NAFLD的细胞模型。与SJP，LY294002（选择性PI3K抑制剂）或该组合共同孵育24小时后，对细胞进行Akt，mTOR，S6，SREBP1-c和FASN的Western印迹检测。结果。 HFD明显诱发肝脂肪变性。在透射电子显微镜下观察到大量的脂滴。肝细胞超微结构变化明显，内质网明显扩张，线粒体收缩，细胞基质凝固。尽管在HFD喂养的大鼠中血清肝酶和组织促炎细胞因子未见差异，但SOD和GSH-px的组织水平低得多，病理损伤严重。但是，SJP处理显着减弱了超微结构的变化，并保护了大鼠肝脏免受炎症性损伤。在油酸处理过的LO2细胞中观察到大量的脂滴和pAkt，pmTOR，pS6和FASN的高表达，而这些变化通过SJP处理得以恢复。结论。 SJP可有效减轻HFD诱导的大鼠NAFLD，这种作用可能部分与抑制Akt / mTOR / S6途径有关。

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