Analysis of the Composition and Anti-Rheumatoid Arthritis Mechanism of Qintengtongbi Decoction Based on Network Pharmacology

Abstract

Qintengtongbi Decoction (QTTBD) is a traditional prescription for rheumatoid arthritis (RA) treatment in Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, southern China's Guangxi Zhuang Autonomous Region. However, there is not yet any analysis on its active compounds or action mechanism for treating RA. Moreover, the prescription has not been investigated from the perspective of network pharmacology. Therefore, this study aimed to analyze the compounds QTTBD and their potential pharmacological effects and the mechanism by which they treat RA via an integrated network pharmacology approach. With the aid of the relevant database tools and research indices, 188 compounds and 272 related drug targets genes/proteins were collected from QTTBD through the compound-target network, and 175 common gene targets between the QTTBD and RA were obtained by Venn 2.1. Finally, the top 10 gene targets and pathways were identified through the protein–protein interaction network, gene ontology, and KEGG pathway analysis: the gene targets include AKT1, IL6, TP53, VEGFA, MAPK3, TNF, CASP3, JUN, EGF, and EGFR; the pathways include oxytocin signaling pathway, amphetamine addiction, graft-versus-host disease, ovarian steroidogenesis, cGMP-PKG signaling pathway, Rap1 signaling pathway, allograft rejection, cytokine–cytokine receptor interaction, regulation of lipolysis in adipocytes and inflammatory mediator regulation of transient receptor potential channels. Therefore, it is concluded that a network pharmacology-based approach can help reveal and clarify the anti-RA role of QTTBD, and provide a scientific basis for further research into the mechanism.

Qinteng Tongbi Decoction Medicated Serum Exerts Regulates the Proliferation, Migration, and Apoptosis of Synovial Fibroblasts in Adjuvant-Induced Arthritis Rats Model via Phosphatidylinositol 3-Kinase/Protein Kinase B Signaling Pathway

“…And the whole formula of QTTBD has the functions of dispelling wind and dampness, dispelling cold and eliminating paralysis, dredging collaterals and relieving pain, and can effectively prevent and treat RA. 9 The results of this recent study showed that compared with the model group, the proliferation of FLS cells in the QTTBD drug-containing serum treatment group was effectively inhibited (p <0 .01), and its apoptosis rate increased significantly (p <0 .05), which was positively correlated with the drug dosage and intervention time; the levels of IL-6, IL-1β, and TNF-α after QTTBD drug-containing serum intervention decreased significantly (p <0 .05), the expression of PI3K, AKT1, p-AKT1, and Bax protein was also lower than that in the model group (p <0 .05), while the expression of Bcl-2 increased (p < 0.05) To sum up, we could conclude that QTTBD could effectively inhibit the level of inflammatory factors of RA, effectively regulate the expression of related proteins, and relieve RA symptoms. However, there are still some problems that require researchers to make breakthroughs in future studies, including the small sample size of clinical case studies of drug treatment RA, role targets related to drug treatment, in-depth research on the mechanism of drug action, etc.…”

“…And the whole formula of QTTBD has the functions of dispelling wind and dampness, dispelling cold and eliminating paralysis, dredging collaterals and relieving pain, and can effectively prevent and treat RA. 9…”

“…Its mechanism might be related to the intervening Oxytocin signaling pathway, cGMP-protein kinase G signaling pathway, Rap1 signaling pathway, PI3K-Akt signaling pathway, mitogen-activated protein kinase (MAPK) signaling pathway, Wnt signaling pathway, and regulating the expression levels of AKT1, interleukin (IL)-1β, IL-2, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma (PIK3CG), tumor necrosis factor (TNF), IL-10, IL-4, IL-6, and other genes. 9 However, after searching the literature, it was found that the research on QTTBD's anti-RA was still in the initial stage, and there has been no report on the relevant pharmacology and the mechanism of its action. Therefore, this recent study mainly aims to report the regulatory effect of QTTBD on the proliferation, migration, and apoptosis of fibroblast-like synovial (FLS) cells in the adjuvant-induced arthritis (AIA) rat model and tries to clarify its anti-RA mechanism for academic exchanges.…”