Relationship between NLRP3 inflammasome-IL-1β axis and End-MT after acute myocardial infarction in rats |
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Authors: | TANG Shi-lin LIU Yi-jian PENG Liang-shan ZHAO Zheng-liang TAN Yi-qing WANG Qiao-sheng |
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Affiliation: | 1. Intensive Care Unit, The First Affiliated Hospital of University of South China, Hengyang 421001, China;2. Department of Cardiology, The Third Hospital of Changsha, Changsha 410015, China |
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Abstract: | AIM: To investigate whether activation of NLRP3 inflammasome-IL-1β axis is consistent with endothelial-mesenchymal transition (End-MT) during the process of myocardial fibrosis after acute myocardial infarction (AMI). METHODS: Adult male SD rats (n=30) were randomly divided into sham operation group (n=15) and AMI group (n=15). After 28 d, Masson staining was used to detect the level of myocardial fibrosis. The activation of NLRP3 inflammasome including NLRP3, ASC, pro-caspase-1 and caspase-1, the endothelial cell markers CD31 and VE-cadherin, and the mesenchymal cell markers α-SMA and FSP1 were analyzed by Western blot. The expression of IL-1β was measured by ELISA. RESULTS: The levels of myocardial fibrosis and End-MT, the activation of NLRP3 inflammasome, and the expression of caspase-1 and IL-1β were significantly increased in AMI group compared with sham operation group (P<0.05). CONCLUSION: The activation of NLRP3 inflammasome-IL-1β axis is significantly consistent with End-MT process, suggesting that NLRP3 inflammasome-IL-1β, as a potential target for the activation of End-MT, will provide a novel theoretical target for the treatment of myocardial fibrosis and heart failure after AMI. |
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Keywords: | NLRP3 inflammasome Interleukin-1β Endothelial-mesenchymal transition Acute myocardial infarction |
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