Network-based analysis and experimental validation explored Bu-Yang-Huan-Wu-Tang protects endothelial cells after hypoxia-reoxygenation injury by inhibiting the PI3K/AKT/FOXO1 pathway
首发时间:2024-03-06
Abstract:Purpose: To explore the drug targets and potential mechanisms of Bu-Yang-Huan-Wu-Tang (BYHWT) in the treatment of acute kidney injury (AKI) through network pharmacology and experimental validation. Methods: A network-based analysis research approach was used to predict the main active ingredients, targets of action and potential signaling pathways of BYHWT for AKI treatment. The protective effect of BYHWT on human umbilical vein endothelial cells (HUVEC) was verified by detecting the PI3K/AKT/FOXO1 signaling pathway and related factors through in vitro experiments. Results:A total of 124 active components of BYHWT were screened, with 444 action targets, 1,708 AKI disease-related target genes, and 210 targets at the intersection of components and diseases were obtained. Through GO and KEGG enrichment analysis, we obtained 219 signaling pathways of BYHWT for the treatment of AKI, and screened the top 10 pathways with the highest degree of enrichment, which involved the PI3K-AKT signaling pathway, and the experimental validation results showed that BYHWT-containing serum increased the expression of p-PI3K, p-AKT, and p-FOXO1, and increased the phosphorylation of FOXO1, and decreased the expression of FOXO1 expression. Conclusion: BYHWT may play a role in ameliorating endothelial cell apoptosis and protecting injured endothelial cells by regulating the PI3K/AKT/FOXO1 pathway.
keywords: AKI Network-based analysis BYHWT hypoxia-reoxygenation HUVEC network analysis
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基于网络药理分析和实验验证补阳还五汤通过抑制PI3K/AKT/FOXO1通路保护缺氧-复氧损伤后的内皮细胞
摘要:目的:通过网络药理学和实验验证,探讨BYHWT在急性肾损伤(AKI)治疗中的药物靶点和潜在机制。方法:采用网络药理学研究方法预测BYHWT治疗AKI的主要活性成分、作用靶点和潜在信号通路。通过体外实验检测PI3K/AKT/FOXO1信号通路及相关因子,验证BYHWT对脐静脉内皮细胞(HUVEC)的保护作用。结果:筛选得到BYHWT活性成分共124个,作用靶点444个,AKI疾病相关靶基因1708个,得到成分与疾病交集靶点210个。通过GO和KEGG富集分析得到BYHWT治疗AKI的219条信号通路,筛选其中富集程度最高的前10条通路,结果涉及PI3K-AKT信号通路。体外实验验证结果,BYHWT含药血清能增加p-PI3K、p-AKT、p-FOXO1的表达,增加FOXO1磷酸化,降低FOXO1表达。结论:BYHWT可能通过调控PI3K/AKT/FOXO1通路发挥改善内皮细胞的凋亡,保护损伤的内皮细胞。
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基于网络药理分析和实验验证补阳还五汤通过抑制PI3K/AKT/FOXO1通路保护缺氧-复氧损伤后的内皮细胞
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