首页|CARD6在脓毒症心肌损伤中的机制研究

CARD6在脓毒症心肌损伤中的机制研究

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目的:探讨CARD6 在脓毒症心肌损伤中的调节机制.方法:将C57BL/6 小鼠随机分为对照组与模型组.采用LPS腹腔注射法构建脓毒症心肌损伤小鼠模型,RT-qPCR检测小鼠心肌组织中CARD6、caspase-1 的mRNA水平.体外实验则采用LPS刺激转染CARD6 过表达质粒的H9C2 细胞,检测caspase-1、细胞活力、CK-MB水平.结果:与对照组相比,模型组小鼠心肌组织中LDH、CK-MB含量,caspase-1 表达水平上升,提示脓毒症导致小鼠心肌损伤,而CARD6 表达水平明显降低.体外实验发现CARD6 表达水平呈下降趋势,转染含有CARD6 的过表达质粒后细胞释放CK-MB的水平降低、细胞活力增加、caspase-1 水平降低.结论:CARD6 可改善脓毒症所致心肌损伤,其机制可能与caspase-1介导的细胞焦亡相关.
Study on the role of CARD6 in the sepsis-induced myocardial injury
Objective:To explore the regulatory mechanism of CARD6 in sepsis-induced myocardial injury.Methods:C57BL/6 mice were randomly divided into a control group and a sepsis model group.A mouse model of sepsis-induced myocardial injury was constructed using LPS intraperitoneal injection method,and the mRNA expression levels of CARD6 and caspase-1 in mouse myocardial tissue were detected by RT-qPCR.In vitro,H9C2 cells were stimulated by LPS and transfected with overexpression plasmid containing CARD6,and the levels of caspase-1,cell viability and CK-MB content were detected.Results:Compared with the control group,the contents of LDH and CK-MB in myocardial tissue of mice increased in the model group,suggesting that sepsis can cause myocardial damage in mice.In addition,the expression level of CARD6 in the cardiac tissue of the model group was significantly reduced.The intracellular CARD6 expression level in the LPS-treated H9C2 cell also showed a downstream trend.After transfection with the overexpression plasmid containing CARD6,the release of CK-MB levels in H9C2 cells decreased,cell viability increased and the expression level of caspase-1 decreased.Conclusion:CARD6 can ameliorate myocardial injury caused by sepsis and its mechanism may be related to caspase-1 mediated pyroptosis.

CARD6caspase-1pyroptosissepsismyocardial damage

李一民、石宁宁、曲央旺姆、辛勇、周吴刚

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日喀则市人民医院重症医学科 日喀则 857000

上海交通大学医学院附属第九人民医院急诊科 上海 200011

CARD6 caspase-1 细胞焦亡 脓毒症 心肌损伤

西藏自治区自然科学基金联合项目西藏自治区自然科学基金组团式医学援藏项目

XZ202101ZR0011GXZ2020ZR-ZY40Z

2024

上海医药
上海医药行业协会

上海医药

影响因子:0.781
ISSN:1006-1533
年,卷(期):2024.45(5)
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