Black ginseng extract alleviates particulate matter-induced airway inflammation by suppressing the ROS/NLRP3/caspase-1 pathway in macrophages

초록

Ethnopharmacological relevance: Black ginseng extract (BGE) is a processed form of ginseng used in East Asian medicine to treat inflammatory respiratory diseases and is known for its excellent bioavailability and pharmacological efficacy. Aim of the study: This study investigates the preventative effects and mechanisms of BGE against inflammatory lung damage caused by particulate matter (PM) in mouse alveolar macrophages (MH-S) and a mouse lung injury model. Materials and methods: Reactive oxygen species (ROS) production and MH-S cell viability were assessed using DCFDA and the Cell Counting Kit-8 assay, respectively. In Balb/c mice exposed to a combination of PM10 and diesel exhaust particles (PM/DEP), various cell types involved in immune cell infiltration were examined through Diff-Quik staining and flow cytometry. Lung histological changes were analyzed using hematoxylin and eosin, Masson's trichrome, and immunofluorescence staining. The molecular mechanism of BGE was investigated via Western blotting, caspase-1 activity assay, secretory/cleaved IL-1 beta ELISA, and real-time qPCR. Results: In PM2.5-stimulated MH-S cells, BGE inhibits inflammation and cellular damage by decreasing ROS levels involved in the NLRP3 inflammasome-mediated pyroptosis. In mice exposed to a PM/DEP, BGE reduces immune cell influx (mainly neutrophils), inflammatory cytokine expression, and abnormal histopathological changes. Notably, BGE administration decreases macrophage activation markers, such as F4/80 and IL-1 alpha, in PM/DEP-exposed lungs. BGE also suppresses the activity of the NLRP3/caspase-1 pathway in mice's lungs. Conclusion: BGE prevents inflammatory lung injury by decreasing ROS levels, thereby inactivating the NLRP3/ caspase-1/pyroptosis pathway both in vitro and in vivo. This study highlights BGE's potential as a natural treatment for PM-induced lung inflammation.

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