Protective effect of oxyberberine against acute lung injury in mice via inhibiting RhoA/ROCK signaling pathway

罗亚 支气管肺泡灌洗 促炎细胞因子 肺水肿 医学 炎症 病理 A549电池 免疫学 化学 信号转导 内科学 生物化学
作者
Baoyi Chen,Shiting Gong,Minhua Li,Yanlu Liu,Juan Nie,Jingna Zheng,Xiaohong Zheng,Jincan Li,Yuxuan Gan,Ziren Su,Jie Chen,Yucui Li,Qingfeng Xie,Fang Yan
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier BV]
卷期号:153: 113307-113307 被引量:4
标识
DOI:10.1016/j.biopha.2022.113307
摘要

Acute lung injury (ALI), hallmarked with alveolar epithelial barrier impairment and pulmonary edema induced by acute inflammation, presents a severe health burden to the public, due to the limited available interventions. Oxyberberine (OBB), having improved anti-inflammatory activity and safety, is a representative component with various activities derived from berberine, whereas its role against ALI with alveolar epithelial barrier injury remains uncertain. To investigate the influence and underlying mechanisms of OBB on ALI, we induced acute inflammation in mice and A549 cells by using lipopolysaccharide (LPS). Changes in alveolar permeability were assessed by analyzing lung histopathology, measuring the dry/wet weight ratio of the lungs, and altering proinflammatory cytokines and neutrophils levels in the bronchoalveolar lavage fluid (BALF). Parameters of pulmonary permeability were assessed through ELISA, western blotting, quantitative real-time PCR, and immunofluorescence analysis. U46619, the agonist of RhoA/ROCK, was employed to further investigate the mechanism of OBB on ALI. Unexpectedly, we found OBB mitigated lung impairment, pulmonary edema, inflammatory reactions in BALF and lung tissue, reduction in ZO-1, and addition of connexin-43. Besides, OBB markedly reduced the expression of RhoA in association with its downstream factors, which are linked to the intercellular junctions and permeability both in vivo and in vitro. Nevertheless, U46619 abolished the benefits obtained from OBB in A549 cells. In conclusion, these outcomes indicated that OBB exerted RhoA/ROCK inhibitor-like effect to moderate alveolar epithelial barrier impairment and permeability, ultimately preventing ALI progression.
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