This study aimed to investigate the anti-inflammatory and antioxidant effects of atractylon on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Changes in lung function parameters were measured in mice after intraperitoneal administration of atractylon. Pathological changes in lung tissue were observed by H&E staining, and the degree of pulmonary edema was assessed by the lung wet/dry weight ratio (W/D). Kit assays were used to detect changes in oxidative stress markers in mouse serum and the protein concentration in bronchoalveolar lavage fluid (BALF). ELISA was employed to measure the expression levels of inflammatory cytokines in BALF and serum. Western blot was used to detect the expression levels of proteins related to the cGAS-STING pathway and vascular cell adhesion molecule-1 (VCAM-1) in lung tissue. Results showed that, compared to the ALI model group, mice in the low-dose and high-dose atractylon groups exhibited significant improvement in lung function parameters, alleviated pulmonary edema, and reduced inflammatory cell infiltration in lung tissue. Protein content and inflammatory cytokine levels in serum and BALF were decreased, while serum oxidative stress indicators were improved. Western blot results further indicated that atractylon could regulate the cGAS-STING pathway, blocking the generation of inflammatory signals, and simultaneously inhibit VCAM-1 expression, thereby reducing pulmonary vascular injury. The results suggest that atractylon may alleviate LPS-induced ALI by modulating the cGAS-STING signaling pathway, reducing the expression of pro-inflammatory cytokines and the production of pro-inflammatory mediators, and improving vascular endothelial injury. This study provides a new potential target and theoretical basis for the treatment of ALI, as well as a potential drug candidate for ALI therapy.

AIM:This study investigates the apoptotic and autophagic effects of atractylodin on lung cancer cells,elucidating the underlying molecular mechanisms.METHODS:Non-small cell lung cancer(NSCLC)A549 and H460 cells,in addition to non-cancerous HBE cells,were cultured in vitro.The effects of atractylodin at various concen-trations on cell viability were assessed using CCK-8 assay.Apoptotic effects were evaluated through Hoechst staining and flow cytometry,while Western blot analysis was performed to detect changes in protein expressions associated with apopto-sis and autophagy,including P62,beclin-1,microtubule-associated protein 1 light chain 3(LC3),Kelch-like epichloro-hydrin(ECH)-associated protein-1(Keap-1),nuclear factor E2-related factor 2(Nrf2),heme oxygenase-1(HO-1),and NAD(P)H:quinone oxidoreductase 1(NQO1).Autophagic flux was further analyzed using acridine orange(AO)stain-ing,and immunofluorescence for LC3 and Nrf2.Additionally,autophagy inhibition experiments were conducted using chloroquine(CQ),followed by analyses of autophagy and apoptosis.Reactive oxygen species(ROS)levels were quanti-fied using DCFH-DA.RESULTS:Treatment with atractylodin significantly reduced the viability of A549 and H460 lung cancer cells,promoting apoptosis and inducing autophagy.This was evidenced by an increase in acidic autophagic vesi-cles,upregulation of LC3 and beclin-1,and downregulation of P62.Inhibition of autophagy by chloroquine reversed atrac-tylodin-induced apoptosis.Moreover,atractylodin heightened ROS production,inhibited Keap-1,and stimulated the ex-pression of Nrf2,HO-1 and NQO1.CONCLUSION:Atractylodin effectively inhibits the proliferation of lung cancer cells by inducing apoptosis and autophagy.These effects are mediated through the modulation of the ROS/Nrf2/HO-1 sig-naling pathway,underscoring its potential as a therapeutic agent in lung cancer treatment.