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大黄素通过抑制 GSDMD 介导的大鼠肺缺血再灌注损伤中的细胞焦亡而发挥作用。

Emodin alleviates lung ischemia-reperfusion injury by suppressing gasdermin D-mediated pyroptosis in rats.

机构信息

Department of Anesthesiology, Suining First People's Hospital, Suining, Sichuan, China.

Department of Emergency, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Clin Respir J. 2023 Mar;17(3):241-250. doi: 10.1111/crj.13582. Epub 2023 Feb 7.

DOI:10.1111/crj.13582
PMID:36751097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9978909/
Abstract

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.

摘要

背景

细胞焦亡是一种与炎症相关的程序性细胞死亡。大黄素已被报道可减轻多种病理过程引起的肺损伤，并减轻不同组织的缺血再灌注（I/R）损伤。

方法

将 Lewis 大鼠分为假手术组、I/R 组和 I/R+大黄素组。大黄素组和 I/R 组大鼠分别于术前 30min 腹腔注射大黄素和磷酸盐缓冲液，然后行左侧开胸术，夹闭左肺门 90min，再灌注 120min。假手术组大鼠通气 210min。检测肺功能、组织学变化、肺水肿和细胞因子水平。采用 Western blot 法检测蛋白水平。免疫荧光染色评估细胞焦亡。

结果

大黄素减轻了 I/R 引起的肺功能障碍、肺损伤和炎症。体内和体外实验均观察到大黄素对 I/R 介导的内皮细胞焦亡具有保护作用。大黄素通过抑制 TLR4/MyD88/NF-κB/NLRP3 通路而发挥作用。

结论

大黄素通过抑制 GSDMD 介导的细胞焦亡减轻大鼠肺缺血再灌注损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/5b0e331fd934/CRJ-17-241-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/cea32514610f/CRJ-17-241-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/7997429f5969/CRJ-17-241-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/c264d4baf40b/CRJ-17-241-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/b4438501bea3/CRJ-17-241-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/47f404d31995/CRJ-17-241-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/5b0e331fd934/CRJ-17-241-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/cea32514610f/CRJ-17-241-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/7997429f5969/CRJ-17-241-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/c264d4baf40b/CRJ-17-241-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/b4438501bea3/CRJ-17-241-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/47f404d31995/CRJ-17-241-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9f/9978909/5b0e331fd934/CRJ-17-241-g003.jpg

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