Affiliation:
1. Department of Anesthesiology Suining First People's Hospital Suining Sichuan China
2. Department of Emergency, The Central Hospital of Wuhan, Tongji Medical College Huazhong University of Science and Technology Wuhan China
3. Department of Proctology Suining First People's Hospital Suining Sichuan China
4. Department of Ophthalmology Suining First People's Hospital Suining Sichuan China
Abstract
AbstractBackgroundPyroptosis refers to programmed cell death associated with inflammation. Emodin has been reported to alleviate lung injuries caused by various pathological processes and attenuate ischemia–reperfusion (I/R) injuries in diverse tissues.MethodsLewis rats were assigned into the sham, the I/R, and the I/R + emodin groups. Emodin and phosphate‐buffered saline were intraperitoneally injected into rats of the emodin group and I/R group for 30 min, respectively. These rats were then subjected to left thoracotomy followed by 90‐min clamping of the left hilum and 120‐min reperfusion. Sham‐operated rats underwent 210‐min ventilation. Lung functions, histological changes, lung edema, and cytokine levels were assessed. Protein levels were measured by western blotting. Immunofluorescence staining was conducted to evaluate pyroptosis.ResultsEmodin alleviated the I/R‐induced lung dysfunction, lung damages, and inflammation. Protective effects of emodin against I/R‐mediated endothelial pyroptosis was observed in vivo and in vitro. Mechanistically, emodin inactivated the TLR4/MyD88/NF‐κB/NLRP3 pathway.ConclusionEmodin attenuates lung ischemia–reperfusion injury by inhibiting GSDMD‐mediated pyroptosis in rats.
Subject
Genetics (clinical),Pulmonary and Respiratory Medicine,Immunology and Allergy
Cited by
2 articles.
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