Anti-Inflammatory Effects of Ginsenosides: Molecular Mechanisms and Network Pharmacology Analysis

Inflammation is a pathological process central to many chronic diseases. Conventional anti-inflammatories, including NSAIDs and corticosteroids, are limited by adverse effects and suboptimal efficacy with long-term use. Ginsenosides from Panax ginseng have emerged as promising multi-target candidates with favorable safety profiles. This review systematically summarizes recent advances in research on the anti-inflammatory pharmacological effects and molecular mechanisms of ginsenosides, with particular emphasis on Rg1, Rb1, Rd, Re, and Rg3. Recent literature was collected and analyzed, and network pharmacology and bioinformatics approaches were employed to predict therapeutic targets and regulatory networks. Core anti-inflammatory mechanisms include suppression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and NF-κB signaling; modulation of TLR4/NF-κB and NLRP3 inflammasome activity; regulation of MAPK (ERK, JNK, and p38) phosphorylation; activation of Nrf2/HO-1 and Hippo-YAP/TAZ pathways; inhibition of COX-2 and iNOS expression; regulation of macrophage polarization; and modulation of membrane permeability and ion exchange. This study elucidates the association between ginsenosides and various inflammatory diseases, systematically consolidating their diverse molecular mechanisms underlying their treatment of typical inflammatory conditions. By integrating modern techniques such as network pharmacology and molecular docking, this review deepens our understanding of the efficacy of ginsenosides in the management of inflammatory diseases. It provides critical insights for further exploration of ginsenosides' pharmacological actions, the development of novel anti-inflammatory drugs, and the interpretation of the modern scientific basis underlying TCM concepts such as ginseng's "restorative and stabilizing" properties.