Protective effect and mechanism of vitexin regulating Epac1 / CaMK Ⅱ pathway on acute myocardial ischemia reperfusion injury in mice
10.19405/j.cnki.issn1000-1492.2023.10.007
- Author:
Qin Gan
1
;
Huanhua Yang
2
;
Lingyu Zhang
2
;
Xiaojia Liu
2
;
Liuyi Dong
2
Author Information
1. Dept of Pharmacology，School of Basic Medicine，Anhui Medical University，Hefei 230032 ; Dept of Basic Medicine，Hefei Technology College，Hefei 230012
2. Dept of Pharmacology，School of Basic Medicine，Anhui Medical University，Hefei 230032
- Publication Type:Journal Article
- Keywords:
vitexin;
Epac1;
CaMK Ⅱ;
myocardial ischemia reperfusion injury
- From:
Acta Universitatis Medicinalis Anhui
2023;58(10):1652-1656
- CountryChina
- Language:Chinese
-
Abstract:
Objective : To investigate the role of Epac1 / CaMK Ⅱ signaling pathway in myocardial ischemia reper- fusion injury (MIRI) in mice，and to investigate the protective effect of vitexin ( VT) on acute MIRI．
Methods:C57 / BL mice were randomly divided into 5 groups : Sham surgery group ( Sham) ，ischemia reperfusion group ( I / R) ，and ischemia reperfusion + vitexin group ( function 3，6，12 mg / kg groups) ．Ligation of the left anterior descending coronary artery (LAD coronary artery) in mice resulted in ischemia of part of the heart tissue for 30min and reperfusion of the blood for 120min．Mouse myocardial ischemia reperfusion injury ( MIRI) model was established．In the sham operation group，only the LAD was not ligated．Serum LDH levels of mice were detected．Hema- toxylin-eosin (H＆E) staining was performed on the left ventricular myocardium of mice to observe the histopatho- logical changes．The expression level of Epac1 in myocardial tissue was observed by immunohistochemistry．The protein expressions of Epac1，Rap1，CaMK Ⅱ and ERK / p-ERK were determined by Western Blot.
Results : Compared with Sham group，serum LDH level of mice in I / R group was significantly increased，protein expressions of Epac1， Rap1 and CaMK Ⅱ in myocardial tissue were significantly up-regulated，and ERK1 /2 phosphorylation level was decreased．Compared with I / R group，vitexin (3，6，12 mg / kg) pretreatment group decreased serum LDH level，inhib- ited Epac1，Rap1 and CaMK Ⅱ protein expression in mouse myocardial tissue，and promoted ERK1 /2 phosphoryla- tion(P＜0. 05 or P＜0. 01) ．The histopathological results showed that the myocardial fibers in the I / R group were disordered and broken，with increased gaps and obvious inflammatory cell infiltration．In the vitexin treatment group，the myocardial fibers were arranged more neatly and inflammatory cells were infiltrated less.
Conclusion:Vitexin may regulate Epac1 / CaMK Ⅱ signaling pathway，down-regulate CaMK Ⅱ protein expression，increase ERK phosphorylation，and effectively reduce MIRI.
- Full text:2024071217505583523牡荆素调控Epac1_Ca...肌缺血再灌注损伤的作用机制_甘琴.pdf
