Emodin alleviates lung ischemia-reperfusion injury by suppressing gasdermin D-mediated pyroptosis in rats
- Clin Respir J. 2023 Feb 7. doi: 10.1111/crj.13582.
- 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.
Background: Pyroptosis 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.
Methods: Lewis 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.
Results: Emodin 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.
Conclusion: Emodin attenuates lung ischemia-reperfusion injury by inhibiting GSDMD-mediated Pyroptosis in rats.
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Research Areas: Cancer
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