Huang Xian-Ju, He Cai-Jing, Liang Shuai, Wang Jing, Li Jun, Yang Guang-Zhong, Zhao Zhang
School of Pharmacy, South-Central University for Nationalities, Wuhan, China.
Department of Anesthesiology Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Front Pharmacol. 2020 Sep 23;11:575772. doi: 10.3389/fphar.2020.575772. eCollection 2020.
Based on the pathological theory of lipid metabolism and using network pharmacology, this study was designed to investigate the protective effect of water extract of (WVBF) on non-alcoholic fatty liver disease (NAFLD) model using LO2 cells and to identify the potential mechanism underlying the effect. The components of were identified from the public database of traditional Chinese medicine systems pharmacology database (TCMSP). Cytoscape software was used to construct the related composite target network. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were carried out for critical nodes. The BioGPS database was used to determine the distribution of the target in tissues and organs. Moreover, the inhibitory effect of was further investigated using an hepatocyte NAFLD model. Fourteen active components were then selected from the 27 known compounds of . The targets of gene enrichment analysis were mainly distributed in the lipid catabolism-related signaling pathway. Network analysis revealed that five target genes of TNF, MAPK8, mTOR, NF-ĸB, and SREBP-1c were key nodes and played important roles in this process. Organ localization analysis indicated that one of the core target site of was liver tissue. The results of the study revealed that WVBF can alleviate the inflammatory response and lipid accumulation in LO2 hepatocytes by inhibiting oxidative stress and the adipocytokine signaling pathway. Genes and proteins related to the lipid synthesis, such as SREBP-1C, acetyl-CoA carboxylase (ACC), and fatty acid synthase (FASN), were significantly decreased, and PPARα expression is significantly increased with WVBF administration. In conclusion, may regulate local lipid metabolism and attenuate oxidative stress and inflammatory factors through the PPARα/SREBP-1c signaling pathway. The present study also indicates that multiple components of regulate multiple targets and pathways in NAFLD. The findings highlight the potential of as a promising treatment strategy for nonalcoholic fatty liver injury.
基于脂质代谢的病理理论并运用网络药理学,本研究旨在探讨[具体药物名称]水提取物(WVBF)对使用LO2细胞的非酒精性脂肪性肝病(NAFLD)模型的保护作用,并确定其潜在作用机制。[具体药物名称]的成分从中药系统药理学数据库(TCMSP)的公共数据库中进行鉴定。使用Cytoscape软件构建相关的复合靶点网络。然后,对关键节点进行基因本体论(GO)和京都基因与基因组百科全书(KEGG)分析。使用BioGPS数据库确定靶点在组织和器官中的分布。此外,使用[具体药物名称]肝细胞NAFLD模型进一步研究其抑制作用。然后从[具体药物名称]的27种已知化合物中选择了14种活性成分。基因富集分析的靶点主要分布在脂质分解代谢相关信号通路中。网络分析显示,TNF、MAPK8、mTOR、NF-κB和SREBP-1c这五个靶基因是关键节点,并在此过程中发挥重要作用。器官定位分析表明,[具体药物名称]的核心靶点部位之一是肝组织。[具体药物名称]的研究结果表明,WVBF可通过抑制氧化应激和脂肪细胞因子信号通路来减轻LO2肝细胞中的炎症反应和脂质积累。与脂质合成相关的基因和蛋白质,如SREBP-1C、乙酰辅酶A羧化酶(ACC)和脂肪酸合酶(FASN),随着WVBF给药而显著降低,并显著增加PPARα表达。总之,[具体药物名称]可能通过PPARα/SREBP-1c信号通路调节局部脂质代谢并减轻氧化应激和炎症因子。本研究还表明,[具体药物名称]的多种成分在NAFLD中调节多个靶点和途径。这些发现突出了[具体药物名称]作为非酒精性脂肪性肝损伤有前景的治疗策略的潜力。