Mediation of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin cardioplegia in rat hearts via upregulating the protein expression of Bcl-2
- VernacularTitle:JAK2/STAT3通过上调Bcl-2蛋白介导TTX心肌保护作用
- Author:
Shengzhong LIU
- Publication Type:Journal Article
- Keywords:
Signal transducer and activator of transcription 3;
Bcl-2;
Apoptosis;
Tetrodotoxin;
Myocardial protection
- From:
Journal of Chongqing Medical University
1986;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin(TTX) cardioplegia in rat hearts.Methods:A total of 24 Wistar rats were randomly divided into Group Control,Group TTX and Group TTX+AG490(n=8).The left ventricular samples in Group Control were collected as pre-ischemia control through thoracotomy.After isolated heart Langendorff and Neely models were established,the rat hearts in Group TTX were continuously perfused with Krebs-Henseleit(K-H) buffer solution for 30 minutes,arrested by TTX cardioplegia(4℃) for 60 minutes,and underwent reperfusion with K-H buffer solution for 60 minutes,then the left ventricular samples were collected for detections.The rat hearts in Group TTX+AG490 were perfused and reperfused with JAK2 inhibitor AG490(5?mol/L) and K-H buffer solution under the same procedure as Group TTX.The protein expression indexes(PEI) of phosphorylated-STAT3(p-STAT3) and B-cell lymphoma-2(Bcl-2) in myocardium were detected by immunohistochemical assay(IHC).The apoptosis index(AI) of cardiomyocyte was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL).The changes of these indexes in three groups were used for comparison.Results:Compared with Group Control,the PEI of p-STAT3 and Bcl-2 in Group TTX and Group TTX+AG490 increased significantly(P
