Study on PPARδ agonists in reducing myocardial ischemia/reperfusion injury through PGC-1/NFRs pathway
10.3969/j.issn.1671-8348.2025.09.009
- VernacularTitle:PPARδ激动剂通过PGC-1/NFRs通路减轻小鼠心肌缺血/再灌注损伤的研究
- Author:
Jianlong LIU
1
;
Mingxiao ZHANG
;
Qingxin TIAN
Author Information
1. 温州医科大学附属第一医院麻醉科,浙江温州 325000
- Keywords:
PPARδ;
mice;
PGC-1;
myocardial ischemia-reperfusion injury;
apoptosis
- From:
Chongqing Medicine
2025;54(9):2048-2053
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of PPARδ agonist pretreatment on mice myocardial is-chemia-reperfusion injury(MI/RI).Methods The mice were divided into the control group(sham operation group),model group(ischemia for 30 min,reperfusion for 24 h),experiment group 1(GW501516,3 mg·kg-1·d-1)and experiment group 2(GW501516,10 mg·kg-1·d-1).LVEF,LVFS,serum CK-MB,LDH and cTnI levels in the mice of each group were measured;the wet-dry myocardial tissue weight ratio was de-tected,the myocardial histomorphology was observed by microscope,the myocardial cellular apoptosis rate was detected by in situ end labeling(TUNEL);Bax and Bcl-2 were detected by Western blot;the mRNA ex-pressions of PGC-1,NFR-1 and NFR-2 were detected by PCR.Results Compared with the control group,the wet-dry weight ratio,myocardial cellular apoptosis rate,CK-MB,LDH,cTnI and Bax protein expressions in the model group were increased,and the Bcl-2 protein expression,LVEF,LVFS,PGC-1 mRNA,NFR-1 mR-NA and NFR-2 mRNA were decreased(P＜0.05).Compared with the model group,the wet-dry weight ratio,myocardial cellular apoptosis rate,CK-MB,LDH,cTnI levels and Bax protein expression in the experimental group 1 and 2 were decreased,while the levels of Bcl-2 protein expression,LVEF,LVFS,PGC-1 mRNA,NFR-1 mRNA and NFR-2 mRNA were significantly increased(P＜0.05).There was no statistically significant difference in the above indicators between the experimental group 1 and 2(P＞0.05).Conclusion PPARδ ag-onist reduces the mitochondrial damage possibly through PGC-1/NFRs signaling pathway,thereby reduces the myocardial cellular apoptosis in mice and ameliorates MI/RI.
