Effect of senescence marker protein 30 on myocardial injury after myocardial infarction in mice through NLRP3 / Caspase1 inflammatory signaling pathway
Journal Title: Journal of Air Force Medical University - Year 2023, Vol 44, Issue 8
Abstract
Objective To investigate the effect of SMP30-/ - on myocardial inflammatory signaling pathways and myocardial injury after acute myocardial infarction (AMI). Methods Thirty wild-type ( WT) C57BL / 6J mice and thirty SMP30-/ - mice were randomly divided into WT sham operation group (WT + Sham group), WT myocardial infarction group (WT + MI group), SMP30-/ - sham operation group ( SMP30-/ - + Sham group), SMP30-/ - myocardial infarction group ( SMP30-/ - + MI group) . The MI groups were treated with ligation of the left anterior descending coronary artery for modeling, while the Sham groups were treated with no ligation. After 28 d of modeling, the small animals were detected by ultrasonography and sacrificed after isoflurane anesthesia for sampling. HE and Masson staining were performed respectively, the content of reactive oxygen species related to oxidative stress was detected by ELISA, and the expression levels of oxidative stress and pyroptosis-related proteins were detected by Western blotting. Results Compared with the WT + Sham group, the expression of SMP30 significantly decreased in the WT + MI group ( P < 0. 05). Compared with the WT + MI group, SMP30-/ - significantly aggravated the cardiac function injury and the degree of myocardial fibrosis in the myocardial infarction area (P < 0. 05, P < 0. 01) in the SMP30-/ - + MI group. Further tests revealed that SMP30-/ - significantly increased myocardial oxidative stress and inflammatory damage in the SMP30-/ - + MI group (P < 0. 05). Conclusion The expression of SMP30 is significantly down-regulated in AMI tissues. SMP30-/ - can aggravate the cardiac function injury in mice with myocardial infarction, enhance the activation of NLRP3 / Caspase1 inflammatory pathway, and lead to further ventricular remodeling.
Authors and Affiliations
JIANG Liqing, ZHANG Bin, ZHU Hanzhao, ZHANG Liyun, JIN Zhenxiao, YU Shiqiang, DUAN Weixun
Keywords
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