Prdx1 Alleviates Cardiomyocyte Apoptosis Through ROS-activated MAPK Pathway During Myocardial Ischemia/reperfusion Injury

Objective This study was designed to investigate the expression change of peroxiredoxin 1(Prdx1)in rat myocardial ischemia/reperfusion injury model,and to explore the correlation of Prdx1 and ROS-activated MAPK pathway in MIRI induced apoptosis.Methods Sixty-four adult Sprague-Dawley rats were randomly divided into eight groups(n = 8 of each group),sham group as control,experiment group underwent 30 min ischemia and 0,2,4,6,8,12,and 24 h reperfusion.The vivo model of MIRI was established by coronary ligation-reperfusion.Cardiomyocytes and H9c2 cells with hypoxia/ reoxygenation(H/R)treatment were utilized to mimic MIRI in vitro.Rats MIRI model was confirmed by Electrocardiogram(ECG).Western Blot andimmunohistochemical assay were used to detect the expressions of Prdx1,MAPK and cleaved caspase-3.The co-localization of Prdx1 and cleaved caspase-3 was detected byimmunofluorescence staining.The level of apoptosis was detected by Flow cytometry and TUNEL.DCFH-DA assay was used to detect intracellular ROS level.Results 1.In vivo,the expression of Prdx1 up-regulated after MIRI and reached the peak at 6 h after reperfusion.The expression of cleaved caspase-3 was similar to the expression of Prdx1,and reached the peak at 6 h after reperfusion.2.In vitro,the expression of Prdx1 and cleaved caspase-3 up-regulated after H/R treatment,especially at 6 h after reoxygenation.3.In vitro,the phosphorylation level of p38 MAPK,JNK and the level of apoptosis declined after treated with inhibitor of MAPK.4.In vitro,after treated with siPrdx1,the ratio of p-p38/p38 and p-JNK/JNK decreased.5.In vitro,after treated with ROS scavenger,the generation of ROS decreased.At the same time,the level of apoptosis declined.Conclusions Prdx1 alleviated cardiomyocyte apoptosis through ROS-activated MAPK pathway during myocardial ischemia/reperfusion injury.