Abstract / Summary
Alkaloids are the primary active ingredients of various traditional Chinese medicines. Preclinical studies show they possess anti-inflammatory, antioxidant, and anti-fibrotic effects in pulmonary fibrosis (PF) models. To evaluate the efficacy and mechanisms of alkaloids against PF by integrating meta-analysis, network pharmacology, and molecular docking. Randomized controlled trials (RCTs) on alkaloid treatment for PF were systematically searched. Methodological quality was assessed with the Cochrane Risk of Bias tool, and data were synthesized using RevMan 5.3 and Stata 15.0. Network pharmacology studies were carried out with the aid of databases such as SwissTargetPrediction and PubChem, primarily to screen predicted targets and enrich relevant pathways. Molecular docking validated core component-target interactions. Thirty-five RCTs (548 animals) showed that alkaloids significantly improved PF-related indicators compared to controls. Network analysis identified AKT1, EGFR, STAT3, and SRC as key targets, implicating pathways such as Phosphatidylinositol 3-kinase (PI3K)-Protein kinase B (Akt), Hypoxia-inducible factor-1 (HIF-1), Focal adhesion, Advanced glycation end-products (AGE)-Receptor for advanced glycation End-products (RAGE), and Mitogen-activated protein kinase (MAPK). Molecular docking confirmed stable binding between core alkaloids and these targets. Alkaloids such as Cepharanthine, Berberine, and Vinpocetine exert multi-target effects in animal models of PF through anti-oxidative, anti-inflammatory, and inhibition of fibroblast activation. Molecular docking indicates that they target ALB, HSP90AA1, ERBB2, and MAPK1. Current evidence is derived mainly from animal and computational studies, necessitating validation through high-quality clinical trials. Nevertheless, existing findings support their potential as an adjunctive therapy.
Primary Source
International immunopharmacology
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