Mechanism of Anchang Decoction in Treatment of Anti-Inflammatory Effect Based on Network Pharmacology, Molecular Docking and Experimental Verification

Abstract

Context A prescription medication called Anchang Decoction (ACD) has anti-inflammatory properties. Objective To evaluate the mechanism of ACD against inflammation. Materials and methods The “pharmacodynamic constituents - potential targets” and “protein interaction networks” were mapped using Cytoscape software and the STRING database, respectively. The degree of binding between important pharmacodynamic components of ACD and possible targets was then examined using molecular docking analysis using Autodock Vina and PyMOL software, and GO and KEGG pathway enrichment analysis using the David database and the Weishengxin online tool. These findings were eventually confirmed in vitro. Results After the intersection of the two, 539 inflammatory targets and 217 related targets, 34 main active components, and 42 potential anti-inflammatory targets were obtained. These include AKT1, MAPK14, SRC, EGFR, GSK3B, MMP9, MMP2, PTGS2, SYK, ESR1, and MMP2 and GO enrichment results. These three key targets are chosen as downstream validation targets for experimental verification. Furthermore, the colonic tissue and mucosa of ACD group were undamaged in comparison to the model group, and there was no sign of inflammatory cell infiltration. According to CCK-8 data, treatment with 20% ACD drug-containing serum resulted in a significant increase in RAW264.7 cell viability (P < 0.05) when compared to the normal serum group; Serum of ACD-containing medication may considerably lower the NO content of macrophage inflammation and prevent the production of inflammatory markers like TNF-α and IL-6 (P < 0.05); The expression levels of AKT1, MAPK14, and SRC proteins were considerably reduced by ACD in RAW264.7 macrophage inflammation, according to Western Blot data (P < 0.05). Discussion and conclusions ACD exerts anti-inflammatory effects through multi-component interaction with the target, and the mechanism may involve the inhibition of the release of inflammatory cytokines by AKT, MAPK and non-receptor tyrosine kinase signaling pathways. Here, the molecular mechanism of ACD against inflammation was partially clarified and experimentally validated, offering theoretical evidence for more effective clinical application.