Fu Tian, Qin Shuiling, He Huajuan, Zhang Kefeng, Zhang Wei, Tang Xin, Wu Wei
School of Pharmacy, Guilin Medical University, Guilin 541199, China.
Pharmacology Laboratory of Prevention and Treatment of High Incidence of Disease, Guilin Medical University, Guilin 541199, China.
Metabolites. 2022 Oct 17;12(10):981. doi: 10.3390/metabo12100981.
The mechanism of action of in the treatment of immune liver injury was systematically analyzed from the perspective of the biological metabolic network by using non-targeted metabolomics combined with biological network analysis tools. A rat model of acute immune hepatic injury was established by Concanavalin A (Con A) and the efficacy of the treatment of acute immune liver injury was judged by gavage of . Liquid chromatography-mass spectrometry (LC-MS)-based plasma metabolomics was used to identify the key metabolites and metabolic pathways for the hepatoprotective effects of . The results demonstrated that reduced the levels of inflammatory parameters, decreased hepatic malondialdehyde levels, and enhanced hepatic antioxidant enzyme activity in animal experiments. The clustering of metabolomic samples showed significant separation in principal component analysis plots and the three groups in PLS-DA and OPLS-DA models could be clearly distinguished in multivariate statistical analysis. Among the 937 total metabolites, 445 metabolites were significantly different between the control and model groups, while 144 metabolites were identified as metabolites with differences between the model and administration groups, and a total of 39 differential metabolites were identified to affect the metabolic levels of the three groups. The differential metabolites were principally involved in the citric acid cycle, glutathione metabolism, vitamin B6 metabolism, and steroid hormone biosynthesis. This study found that can significantly inhibit acute liver injury in rats, and exert a hepatoprotective effect through anti-inflammatory effect, inhibition of lipid peroxidation, improvement of the antioxidant defense system, and regulation of metabolites and related metabolic pathways. This study will provide a theoretical basis for the application of in the treatment of the liver injury.
采用非靶向代谢组学结合生物网络分析工具，从生物代谢网络的角度系统分析了[药物名称]治疗免疫性肝损伤的作用机制。通过刀豆蛋白A（Con A）建立大鼠急性免疫性肝损伤模型，并通过灌胃[药物名称]来判断其对急性免疫性肝损伤的治疗效果。基于液相色谱-质谱联用（LC-MS）的血浆代谢组学用于鉴定[药物名称]肝保护作用的关键代谢物和代谢途径。结果表明，在动物实验中[药物名称]降低了炎症参数水平，降低了肝脏丙二醛水平，并增强了肝脏抗氧化酶活性。代谢组学样本的聚类在主成分分析图中显示出明显的分离，在偏最小二乘判别分析（PLS-DA）和正交偏最小二乘判别分析（OPLS-DA）模型中的三组在多元统计分析中可以清晰区分。在总共937种代谢物中，对照组和模型组之间有445种代谢物存在显著差异，而模型组和给药组之间有144种代谢物被鉴定为有差异的代谢物，总共鉴定出39种差异代谢物影响三组的代谢水平。差异代谢物主要参与柠檬酸循环、谷胱甘肽代谢、维生素B6代谢和类固醇激素生物合成。本研究发现[药物名称]可显著抑制大鼠急性肝损伤，并通过抗炎作用、抑制脂质过氧化、改善抗氧化防御系统以及调节代谢物和相关代谢途径发挥肝保护作用。本研究将为[药物名称]在肝损伤治疗中的应用提供理论依据。
