| Literature DB >> 32492627 |
Ruimin Guo1, Yanjun Li2, Min Han3, Jun Liu4, Yanni Sun5.
Abstract
Acute lung injury (ALI) is a major cause of sepsis-induced acute respiratory failure. Emodin has been considered to play a protective role for acute lung edema in cecal ligation and puncture (CLP)-induced sepsis model. In this study we aimed to investigate whether emodin could improve CLP-induced lung sepsis via regulating aquaporin (AQP) and tight junction (TJ), inflammatory factors, and pulmonary apoptosis. The results showed that sepsis-induced pulmonary pathological changes were significantly improved after emodin treatment. Emodin was found to upregulate AQP and TJ expression in the CLP model. Meanwhile, inflammatory cytokine release and pulmonary apoptosis was remarkably reduced after emodin treatment in lung sepsis. Our data demonstrated that emodin could suppresse inflammation, restore pulmonary epithelial barrier and reduce mortality in CLP-induced ALI, suggesting the potential therapeutic application of emodin in sepsis.Entities:
Keywords: Acute lung injury; Aquaporin; Inflammatory factor; Pulmonary apoptosis; Tight junction protein
Mesh:
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Year: 2020 PMID: 32492627 DOI: 10.1016/j.intimp.2020.106626
Source DB: PubMed Journal: Int Immunopharmacol ISSN: 1567-5769 Impact factor: 4.932