Mechanism of bulleyaconitine A in inhibiting bone destruction of rheumatoid arthritis via Src/PI3K/Akt signaling pathway

• Published in: Zhongguo zhongyao zazhi Vol. 49; no. 6; p. 1438
• Main Authors: Huang, Feng-Yu, Guo, Wan-Yi, Chen, Pei-Ping, Zhang, Xin-Zhuo, Li, Zhuo-Hang, Huang, He-Lan, Lin, Na, Su, Xiao-Hui, Kong, Xiang-Ying
• Format: Journal Article
• Language: Chinese
• Published: China 01.03.2024
• Subjects: Aconitine - analogs & derivatives; Animals; Arthritis, Experimental; Arthritis, Rheumatoid - drug therapy; Arthritis, Rheumatoid - genetics; Drugs, Chinese Herbal - pharmacology; Molecular Docking Simulation; Phosphatidylinositol 3-Kinases - genetics; Proto-Oncogene Proteins c-akt - genetics; RNA, Messenger; Signal Transduction; Src/PI3K/Akt signaling pathway; bulleyaconitine A; rheumatoid arthritis; bone destruction
• ISSN: 1001-5302
• DOI: 10.19540/j.cnki.cjcmm.20231205.403

Based on the sarcoma receptor coactivator(Src)/phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt) signaling pathway, the mechanism of action of bulleyaconitine A in the treatment of bone destruction of experimental rheumatoid arthritis(RA) was explored. Firstly, key targets of RA bone destruction were collected through GeneCards, PharmGKB, and OMIM databa-ses. Potential targets of bulleyaconitine A were collected using SwissTargetPrediction and PharmMapper databases. Next, intersection targets were obtained by the Venny 2.1.0 platform. Protein-protein interaction(PPI) network and topology analysis were managed by utilizing the STRING database and Cytoscape 3.8.0. Then, Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment analyses were conducted in the DAVID database. AutoDock Vina was applied to predict the molecular docking and binding ability of bulleyaconitine A with key targets. Finally, a receptor activator of nuclear factor-κB(RANKL)-induced osteoclast differentiation mo