Comparative transcriptomics and network pharmacology analysis to identify the potential mechanism of celastrol against osteoarthritis

医学 雷公藤醇 PI3K/AKT/mTOR通路 小桶 转录组 计算生物学 生物 信号转导 基因 遗传学 基因表达 细胞凋亡
作者
Siming Dai,Hui Wang,Meng Wang,Yue Zhang,Zhiyi Zhang,Zhiguo Lin
出处
期刊:Clinical Rheumatology [Springer Science+Business Media]
卷期号:40 (10): 4259-4268 被引量:16
标识
DOI:10.1007/s10067-021-05726-3
摘要

Celastrol is a promising therapeutic agent for the treatment of osteoarthritis (OA). However, the mechanism of action of celastrol is unclear. This study was aiming to identify the potential function of celastrol on OA and determine its underlying mechanism. Celastrol targets were collected from web database searches and literature review, while pathogenic OA targets were obtained from Online Mendelian Inheritance in Man (OMIM) and GeneCards databases. Transcriptomics data was sequenced using an Illumina HiSeq 4000 platform. Celastrol-OA overlapping genes were then identified followed by prediction of the potential function and signaling pathways associated with celastrol using gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. A celastrol-target network was constructed to identify the candidate core targets of celastrol. The predictions were then validated by performing molecular docking and molecular dynamics simulation studies. In total, 96 genes were identified as the putative celastrol targets for treatment of OA. These genes were possibly involved in cell phenotype changes including response to lipopolysaccharide and oxidative stress as well as in cell apoptosis and aging. The genes also induced the mTOR pathway and AGE-RAGE signaling pathway at the intracellular level. Additionally, results indicated that 13 core targets including mTOR, TP53, MMP9, EGFR, CCND1, MAPK1, STAT3, VEGFA, CASP3, TNF, MYC, ESR1, and PTEN were likely direct targets of celastrol in OA. Finally, mTOR was determined as the most likely therapeutic target of celastrol in OA. This study provides a basic understanding and novel insight into the potential mechanism of celastrol against OA.
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