斯特里奇尼精液与白术通过调节细胞凋亡减轻类风湿关节炎的症状

IF 1.5 4区 医学 Q4 CHEMISTRY, MEDICINAL Current computer-aided drug design Pub Date : 2024-01-01 DOI:10.2174/1573409919666230807154555
Xiaoxin Wang, Yuling Li, Huihui Lou, Zidong Yang, Jing Wang, Xiaodong Liang, Yuejuan Bian
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引用次数: 0

摘要

背景:类风湿关节炎(RA)是一种慢性自身免疫性疾病,可导致关节疼痛和残疾,严重影响患者的生活质量。类风湿性关节炎(RA)是一种慢性自身免疫性疾病,可导致关节疼痛和残疾,严重影响患者的生活质量。类风湿性关节炎精液与白术(SA)合用对RA有明显疗效,且类风湿性关节炎精液(SS)不会中毒。然而,其药理机制仍不清楚:本研究旨在探讨Strychni Semen与白术(SA)联合治疗RA的药理机制:方法:我们利用网络药理学筛选SA的活性成分,并预测涉及的靶点和途径。方法:我们利用网络药理学筛选南洋杉的活性成分,并预测相关靶点和通路,然后通过动物实验验证网络药理学的结果:结果:网络药理学发现了 81 种 SA 的活性成分和 141 个靶点;还发现了 2640 个疾病相关基因。SA治疗RA的核心靶点包括ALB、IL-6、TNF和IL-1β。通过基因本体(GO)富集分析,共鉴定出 354 个基因本体术语。京都基因组百科全书(KEGG)通路富集分析结果显示,SA在治疗RA的过程中与TNF信号通路密切相关。此外,根据网络药理学的预测结果,我们建立了佐剂性关节炎(AA)大鼠模型进行体内实验。分析表明,各治疗组均不同程度地改善了AA大鼠的爪肿、免疫器官系数和滑膜组织形态,抑制了IL-1β、TNF-α和IL-6的表达水平,上调了Fas、Bax和Caspase 3的水平,下调了Fas-L、Bcl-2和p53的表达水平:结论:SA具有抗RA作用,SA对AA大鼠的治疗作用机制与细胞凋亡信号通路的调节有关。
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Strychni Semen Combined with Atractylodes Macrocephala Koidz Attenuates Rheumatoid Arthritis by Regulating Apoptosis.

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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来源期刊
Current computer-aided drug design
Current computer-aided drug design 医学-计算机:跨学科应用
CiteScore
3.70
自引率
5.90%
发文量
46
审稿时长
>12 weeks
期刊介绍: Aims & Scope Current Computer-Aided Drug Design aims to publish all the latest developments in drug design based on computational techniques. The field of computer-aided drug design has had extensive impact in the area of drug design. Current Computer-Aided Drug Design is an essential journal for all medicinal chemists who wish to be kept informed and up-to-date with all the latest and important developments in computer-aided methodologies and their applications in drug discovery. Each issue contains a series of timely, in-depth reviews, original research articles and letter articles written by leaders in the field, covering a range of computational techniques for drug design, screening, ADME studies, theoretical chemistry; computational chemistry; computer and molecular graphics; molecular modeling; protein engineering; drug design; expert systems; general structure-property relationships; molecular dynamics; chemical database development and usage etc., providing excellent rationales for drug development.
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