首页|Mn3O4纳米酶处理对缺氧/复氧心肌细胞HIF-1α/BNIP3信号通路的影响

Mn3O4纳米酶处理对缺氧/复氧心肌细胞HIF-1α/BNIP3信号通路的影响

Mn3O4 nanoenzyme treatment alleviates hypoxia/reoxygenation-induced cardiomyocyte injury via HIF-1α/BNIP3 signaling pathway

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目的:探讨四氧化三锰(Mn3O4)纳米酶处理对缺氧/复氧(H/R)心肌细胞低氧诱导因子-1α(HIF-1α)/B淋巴细胞瘤-2/腺病毒E1B 19kDa相互作用蛋白 3(BNIP3)信号通路的影响.方法:建立H9C2 大鼠心肌细胞H/R损伤模型,将H9C2 大鼠心肌细胞随机分为对照组、模型组、四氧化三锰纳米颗粒(Mn3O4 NP)组、二甲氧基雌二醇(2-ME2)组和Mn3O4 NP+2-ME2 组.CCK-8 法检测细胞活力.生化法检测丙二醛(MDA)、乳酸脱氢酶(LDH)水平.Western blot和实时荧光定量PCR分别检测HIF-1α、BNIP3、苄氯素 1(Beclin-1)、家蚕隔离体蛋白1(P62)的蛋白质和mRNA表达水平.结果:与对照组相比,模型组心肌细胞活力下降,LDH及MDA表达水平升高,HIF-1α、BNIP3、Beclin-1 蛋白及mRNA表达水平升高,P62 表达水平降低(P均<0.05).与模型组相比,Mn3O4 NP组心肌细胞活力上升,LDH及MDA表达水平降低,HIF-1α、BNIP3、Beclin-1 蛋白及mRNA表达水平升高,P62 表达水平降低(P均<0.05),2-ME2 组变化相反(P均<0.05).与Mn3O4 NP+2-ME2 组相比,Mn3O4 NP组心肌细胞活力上升,LDH及MDA表达水平降低,HIF-1α、BNIP3、Beclin-1 表达水平升高,P62 表达水平降低(P均<0.05),2-ME2 组变化相反(P均<0.05).结论:Mn3O4 NP可能通过激活HIF-1α/BNIP3信号通路促进H9C2心肌细胞自噬,从而减轻H/R诱导的心肌损伤.
Objective:To explore the effect of Mn3O4 nanoenzyme treatment on HIF-1α/BNIP3 signaling pathway in hypoxia/reoxygenation(H/R)cardiomyocytes.Methods:After establishing a H/R injury model using H9C2 mice,cardiomyocytes were randomly divided into five groups:control group,model group,Mn3O4 NP group,2-ME2 group and Mn3O4 NP+2-ME2 group.In each group,CCK-8 technique was used to determine myocardial cell viability,and Western blot and qRT-PCR were used to detect the protein and mRNA expression levels of HIF-1α,BNIP3,Beclin-1,P62,respectively.MDA and LDH levels were assessed by biochemical methods.Results:Compared with the control group,myocardial cell viability was decreased,LDH and MDA levels were increased,HIF-1α,BNIP3,Beclin-1 protein and mRNA expression levels were increased,and P62 expression was reduced in the model group(P<0.05).Compared with the model group,myocardial cell viability was increased,LDH and MDA levels were decreased,HIF-1α,BNIP3 and Beclin-1 expression levels were increased,and P62 expression was decreased in the Mn3O4 NP group(P<0.05).Opposite changes occurred in the 2-ME2 group(P<0.05).Compared with the Mn3O4 NP+2-ME2 group,myocardial cell viability was increased,LDH and MDA levels were decreased,HIF-1α,BNIP3 and Beclin-1 expression levels were increased,and P62 expression was reduced in the Mn3O4 NP group(P<0.05).Opposite changes were detected in the 2-ME2 group(P<0.05).Conclusion:Mn3O4 NP may promote autophagy of H9C2 cardiomyocytes by activating HIF-1α/BNIP3 signaling pathway,thereby alleviating H/R-induced myocardial injury.

NanoparticleTrimanganese tetraoxideHypoxia/reoxygenation injury

梁慧萍、韩轩茂、蔺雪峰

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014040 内蒙古科技大学包头医学院研究生院

014010 内蒙古科技大学包头医学院第一附属医院心内一科

纳米酶 四氧化三锰 缺氧/复氧损伤

内蒙古自治区自然科学基金项目

2023MS08040

2024

国际心血管病杂志
上海市医学科学技术情报研究所

国际心血管病杂志

CSTPCD
影响因子:0.891
ISSN:1673-6583
年,卷(期):2024.51(5)