衰老标记蛋白30介导四氢姜黄素抗心肌缺血再灌注损伤的机制研究

李晓康; 杨羽淇; 苏小花

doi:10.12125/j.chj.202109052

衰老标记蛋白30介导四氢姜黄素抗心肌缺血再灌注损伤的机制研究

Tetrahydrocurcumin attenuates myocardial ischemia/reperfusion injury via SMP30 and inhibition of cardiomyocyte apoptosis

摘要

摘要:
目的探讨衰老标记蛋白30（SMP30）在四氢姜黄素（THC）抗心肌缺血再灌注（MI/R）损伤中的作用。
方法构建H9c2细胞缺氧/复氧模型和小鼠MI/R模型，利用腺病毒和短发夹RNA（shRNA），在细胞和动物水平下调心肌的SMP30的表达，通过CCK8细胞活力试剂盒、ANNEXIN V- FITC/PI凋亡试剂盒、乳酸脱氢酶（LDH）活性试剂盒、肌酸激酶同功酶（CK-MB）试剂盒、心脏超声等方法，评价细胞活性和心脏功能。
结果敲低SMP30水平后，THC对H9c2细胞的保护作用被部分逆转，THC抗H/R诱发的H9c2细胞死亡能力被削弱；SMP30通过Bax/Blc2途径介导THC对H9c2细胞的保护；THC能够显著改善小鼠MI/R后心脏功能，敲低小鼠心脏SMP30水平后，THC的心脏保护作用被部分逆转。
结论 SMP30参与介导THC抗I/R诱发的心肌细胞凋亡。

Abstract:
AIM To explore the effects of senescence marker protein 30 (SMP30) and tetrahydrocurcumin (THC) in myocardial ischemia/reperfusion injury.
METHODS With H9c2 cells H/R and mice MI/R model, adenovirus and shRNA were used to down-regulate the expression of SMP30 in H9c2 cells and myocardium. CCK8 assay, PI/Annexin V assay, LDH release and CK-MB activity were used to evaluate the apoptosis of H9c2 cells and cardiomyocytes, respectively.
RESULTS After knocking down the level of SMP30, the protective effect of THC on H9c2 cells was partially reversed. THC could significantly improve the cardiac functions after MI/R in mice. Knocking down the level of SMP30 in mouse heart, the MI/R protective effect of THC was partially reversed.
CONCLUSION THC attenuates MI/R injury via SMP30 and inhibition of cardiomyocyte apoptosis

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