通过串联质量标签定量蛋白质组分析、网络药理学分析和实验验证揭示黄连对局灶节段性肾小球肾炎大鼠的药理机制

Wan Feng, Yang Ruchun, Tang Yuewen
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引用次数: 0

摘要

目的:探讨()的分子机制:探索()的分子机制:我们采用基于串联质量标签的定量蛋白质组学方法来确定差异表达的蛋白质。采用网络药理学分析方法分析了()的主要成分并构建了化合物-靶标网络。Western 印迹和定量实时聚合酶链反应(qRT-PCR)用于验证分析结果:结果:在局灶节段性肾小球透明症(FSGS)大鼠体内,凝血酶原-1(TSP-1)和转化生长因子(TGF)-β1/Smad3信号通路蛋白的表达水平显著上调。原癌基因能降低 TSP-1 和 TGF-β1 信号通路蛋白的表达水平。网络药理学分析表明,原儿茶醛是主要的活性成分。随后的实验验证了蛋白质组学和网络药理学分析的结果:我们的研究结果表明,原儿茶醛可通过抑制 TSP-1 激活的 TGF-β1 信号传导来抑制肾硬化,并有可能应用于 FSGS 的治疗。
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Uncovering pharmacological mechanisms of Phellinus linteus on focal segmental glomeruloscleosis rats through tandem mass tag-based quantitative proteomic analysis, network pharmacology analysis and experimental validation.

Objective: To explore the underlying molecular mechanism of ().

Methods: We used a tandem mass tag-based quantitative proteomic method to determine the differentially expressed proteins. Network pharmacology analysis was used to analysis the main components of and construct the compound-target network. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were used to validate the analyses results.

Results: The expression levels of thrombospondin-1 (TSP-1) and transforming growth factor (TGF)-β1/Smad3 signaling pathway proteins were significantly upregulated in focal segmental glomeruloscleosis (FSGS) rats. The reduced the expression levels of TSP-1 and TGF-β1 signaling pathway proteins. Network pharmacology analysis revealed that protocatechualdehyde was the main active component. Subsequent and experiments validated the results of proteomic and network pharmacology analyses.

Conclusions: Our results suggested that may inhibit renal sclerosis by inhibiting TSP-1-activated TGF-β1 signaling and may have potential applications in the treatment of FSGS.

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