作者
Jinchao Zhu,Ningning Shao,Zeyu Huang,Yanqing Liu,Xiangyan Meng,Ziquan Liu,Yujie Sun,Jinrui Dong,Haojun Fan
摘要
OBJECTIVES: powder (UXP) against lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the underlying mechanism. METHODS: =6) for 6 consecutive days, starting on the day of modeling. After the treatment, the lung wet-to-dry (W/D) ratios were determined, inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were measured by ELISA, and inflammatory cell infiltration was assessed by flow cytometry. Histopathological injury of the lungs was observed using HE staining, and pulmonary SOD, MDA, and GSH levels were determined. Pulmonary mRNA expressions of inflammatory mediators were quantified by RT-qPCR, and NF‑κB and STAT3 activation was analyzed using Western blotting; mitochondrial ultrastructure was examined with transmission electron microscopy. In a LPS-stimulated BEAS-2B cell model, the effects of UXP and DEX were assessed on cell viability, apoptosis, reactive oxygen species (ROS), mitochondrial function, lipid peroxidation, and ferrous iron levels. RESULTS: The LPS-challenged mice exhibited a higher lung W/D ratio and increased BALF cytokine levels and inflammatory cell counts with pronounced lung inflammation and tissue damage, lowered SOD and GSH levels, elevated MDA levels, increased mRNA expressions of inflammatory mediators and the p-NF‑κB/NF‑κB and p-STAT3/STAT3 ratios, and obvious mitochondrial damages. UXP markedly alleviated these changes with an efficacy comparable to DEX. In LPS-stimulated BEAS-2B cells, UXP significantly improved cell viability, redcued cell apoptosis and ROS accumulation, preserved mitochondrial integrity, and reduced lipid peroxidation and ferroptosis-associated changes. CONCLUSIONS: UXP has strong protective effects against LPS-induced ALI in mice possibly by suppressing inflammation, oxidative stress, ferroptosis, and apoptosis, modulating the NF‑κB/STAT3 signaling axis, and maintaining mitochondrial integrity.