Naloxone Postconditioning Alleviates Rat Myocardial Ischemia Reperfusion Injury by Inhibiting JNK Activity.
10.4196/kjpp.2014.18.1.67
- Author:
Anzhou XIA
1
;
Zhi XUE
;
Wei WANG
;
Tan ZHANG
;
Tiantian WEI
;
Xingzhi SHA
;
Yixun DING
;
Weidong ZHOU
Author Information
1. Department of Pharmacology, Xuzhou Medical College, Xuzhou 221004, Jiangsu Province, China.
- Publication Type:Original Article
- Keywords:
Cell apoptosis;
c-Jun N-terminal kinases (JNK);
Ischemia reperfusion;
Naloxone
- MeSH:
Animals;
Apoptosis;
Blotting, Western;
Humans;
In Situ Nick-End Labeling;
Ischemia;
JNK Mitogen-Activated Protein Kinases;
Male;
Myocardial Ischemia*;
Myocytes, Cardiac;
Naloxone*;
Rats*;
Rats, Sprague-Dawley;
Reperfusion Injury*;
Reperfusion*
- From:The Korean Journal of Physiology and Pharmacology
2014;18(1):67-72
- CountryRepublic of Korea
- Language:English
-
Abstract:
To investigate the alteration of c-Jun N-terminal kinase (JNK) activity after myocardial ischemia reperfusion injury (MIRI) and further explore the effect of naloxone postconditioning on MIRI. Forty male Sprague Dawley rats were randomly divided into five groups: sham operation (sham, n=8); ischemia reperfusion (IR, n=8); IR+naloxone 0.5 mg/kg (Nal L, n=8); IR+naloxone 1.0 mg/kg (Nal M, n=8); IR+naloxone 2.0 mg/kg (Nal H, n=8). Pathological changes of myocardial tissue were visualized by HE staining. The expression of p-JNK, and the apoptosis of cardiomyocytes were investigated with Western blotting and the TUNEL assay, respectively. Irregular arrangement and aberrant structure of myocardial fibers, cardiomyocytes with granular or vacuolar degeneration, and inflammatory cells infiltrating the myocardial interstitial regions characterized MIRI in the IR group. Signs of myocardial injury and inflammatory infiltration were less prominent in the Nal-treated groups. The expression of p-JNK in the sham group and in all Nal-treated groups was significantly lower than that in the IR group (p<0.01). The apoptosis index of cardiomyocytes in the IR group was significantly higher than in the sham group (p< 0.01). The apoptosis indices of cardiomyocytes in all Nal-treated groups were significantly reduced to 55.4%, 26.2%, and 27.6%, respectively, of the IR group (p< 0.01). This study revealed that Naloxone postconditioning before reperfusion inhibits p-JNK expression and decreases cell apoptosis, thus alleviating MIRI.
