Lipidomic Analysis of the Protective Effects of Shenling Baizhu San on Non-Alcoholic Fatty Liver Disease in Rats
Lipidomic Analysis of the Protective Effects of Shenling Baizhu San on Non-Alcoholic Fatty Liver Disease in Rats
复制标题
参苓白术散对大鼠非酒精性脂肪肝保护作用的脂质组学分析
DOI：
10.3390/molecules24213943
复制
发表时间：
2019-11-01
期刊：
影响因子：
4.6
通讯作者：
Yang, Qinhe
中科院分区：
文献类型：
--
作者：
Deng, Yuanjun;Pan, Maoxing;Yang, Qinhe
参苓白术散（SLBZS）是著名的中药，对非酒精性脂肪性肝病（NAFLD）有一定的保护作用，但其确切机制尚不清楚。本研究的目的是利用脂质组学研究SLBZS在大鼠NAFLD模型中的保护作用的机制，并评估Sirtuin 1（SIRT 1）在SLBZS抗NAFLD机制中的作用。采用高脂饲料诱导大鼠NAFLD模型。应用基于超高效液相色谱-质谱（UHPLC-MS）的非靶向脂质组学方法分析肝脏脂质变化，并使用SIRT 1选择性抑制剂EX 527抑制肝脏中的SIRT表达。结果表明，SLBZS对NAFLD具有保护作用。脂质组学分析表明，30种脂质的有效调节SLBZS管理在高脂饮食大鼠。通路分析表明，甘油磷脂代谢和甘油脂代谢是参附保肾汤抗NAFLD作用机制中密切相关的潜在靶向通路。此外，SLBZS对肝脂肪变性，一些生化参数和肝脏脂质种类的有益作用部分被SIRT 1抑制减弱。总之，我们的研究结果表明，SLBZS管理可以有效地改变一些肝脏脂质种类喂养高脂饮食，这主要是与调节甘油磷脂和甘油脂代谢。此外，SLBZS对肝脏脂质代谢的有益作用可能至少部分归因于肝脏中的SIRT 1活化。
Shenling Baizhu San (SLBZS), a famous traditional Chinese medicine, has been demonstrated to exert protective effects against non-alcoholic fatty liver disease (NAFLD), but its exact mechanisms have not been well understood. The aim of this study was to investigate the mechanisms underlying the protective effects of SLBZS in a rat model of NAFLD using lipidomics and to evaluate the role of Sirtuin 1 (SIRT1) in the mechanism of SLBZS against NAFLD. The rat model of NAFLD was induced by high-fat feeding. An ultra-performance liquid chromatography-mass spectrometry (UHPLC-MS)-based untargeted lipidomics approach was applied to analyze hepatic lipid alterations, and the SIRT1-selective inhibitor EX 527 was used to inhibit SIRT expression in the liver. The results of body and biochemical parameters, as well as histological changes, indicated that SLBZS administration exerted protective effects against NAFLD. Lipidomic analysis showed that 30 lipid species were effectively regulated by SLBZS administration in rats fed a high-fat diet. Pathway analysis indicated that glycerophospholipid metabolism and glycerolipid metabolism were potential target pathways closely involved in the mechanism of SLBZS against NAFLD. Moreover, the beneficial effects of SLBZS on hepatic steatosis, some biochemical parameters and hepatic lipid species were partly diminished by SIRT1 inhibition. In conclusion, our results suggested that SLBZS administration could effectively alter some hepatic lipid species in rats fed a high-fat diet, which was mainly associated with the regulation of glycerophospholipid and glycerolipid metabolism. Furthermore, the beneficial effects of SLBZS on hepatic lipid metabolism may be at least partly attributed to SIRT1 activation in the liver.