ArticleJournal of natural medicines2026
Liang-Ge-San, a classic Chinese prescription, stimulates macrophage-secreted exosomal miR-21 to ameliorate lipopolysaccharide-induced acute lung injury through the regulation of PTEN/PI3K/AKT signaling.
Article in Journal of natural medicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an acute respiratory disorder for which there are no approved drugs with proven efficacy in its treatment. Liang-Ge-San (LGS), a classic Chinese prescription, is generally employed for treating respiratory diseases, including ALI. To elaborate on the therapeutic benefits and potential mechanism of LGS against ALI, the function of exosomal miR-21 in intercellular communication after LGS treatment was assessed by constructing the co-culture system between RAW 264.7 and the mouse type II alveolar epithelial (MLE-12) cells. LPS was employed through intratracheal instillation for constructing an ALI mice model to study the effect of LGS-stimulated exosomal miR-21. LGS suppressed the levels of pro-inflammatory cytokines and enhanced the expression of miR-21 in RAW 264.7 cells, which could be counteracted by the inhibition of miR-21. Moreover, LGS treatment enhanced the secretion of exosomes (referred to as LGS-exosomes) in RAW 264.7 cells, which were enriched with miR-21. MLE-12 cells were capable of internalizing LGS-exosomes, which was inhibited by exosome secretion inhibitor GW4869. Dual luciferase reporter assay exhibited direct PTEN mRNA inhibition by miR-21. LGS-exosomes markedly increased the protein expression of PI3K and p-AKT (Ser473), and decreased the protein expression of PTEN, as well as the pro-inflammatory cytokines in MLE-12 cells. In LPS-induced ALI mice, LGS-exosomes alleviated lung injury and edema, while simultaneously boosting the levels of miR-21 and regulating the proteins involved in the PTEN/PI3K/AKT pathway. LGS protects against LPS-induced ALI by upregulating macrophage-secreted exosomal miR-21 and subsequently regulating the PTEN/PI3K/AKT signaling pathway. Our study offers valuable insights for clinical application of LGS to treat ALI.
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