小桶
类风湿性关节炎
医学
Fas配体
药理学
关节炎
中医药
系统药理学
传统医学
细胞凋亡
免疫学
基因
生物
基因表达
基因本体论
生物化学
替代医学
药品
病理
程序性细胞死亡
作者
Xiaoxin Wang,Yuling Li,Hanning Lou,Zidong Yang,Jing Wang,Xiaodong Liang,Yuejuan Bian
出处
期刊:Current Computer - Aided Drug Design
[Bentham Science]
日期:2024-10-01
卷期号:20 (5): 518-533
标识
DOI:10.2174/1573409919666230807154555
摘要
Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease that can lead to joint pain and disability, and seriously impact patients' quality of life. Strychni Semen combined with Atractylodes Macrocephala koidz (SA) have pronounced curative effect on RA, and there is no poisoning of Strychni Semen (SS). However, its pharmacological mechanisms are still unclear. Objective: In this study, we aimed to investigate the pharmacological mechanisms of Strychni Semen combined with Atractylodes Macrocephala Koidz (SA) for the treatment of RA. Methods: We used network pharmacology to screen the active components of SA and predict the targets and pathways involved. Results originating from network pharmacology were then verified by animal experiments. Results: Network pharmacology identified 81 active ingredients and 141 targets of SA; 2640 disease- related genes were also identified. The core targets of SA for the treatment of RA included ALB, IL-6, TNF and IL-1β. A total of 354 gene ontology terms were identified by Gene ontology (GO) enrichment analysis. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis results showed that SA was closely associated with TNF signaling pathways in the treatment of RA. Furthermore, according to the predicted results of network pharmacology, we established a rat model of Adjuvant Arthritis (AA) for in vivo experiments. Analysis showed that each treatment group led to an improvement in paw swelling, immune organ coefficient and synovial tissue morphology in AA rats to different degrees, inhibit the expression levels of IL-1β, TNF-α and IL-6, upregulated the levels of Fas, Bax and Caspase 3, down-regulated the expression levels of Fas-L, Bcl-2 and p53. Conclusion: SA has an anti-RA effect, the mechanism underlying the therapeutic action of SA in AA rats was related to the regulation of apoptosis signaling pathways
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