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Xia, Anzhou,Xue, Zhi,Wang, Wei,Zhang, Tan,Wei, Tiantian,Sha, Xingzhi,Ding, Yixun,Zhou, Weidong The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.1
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.
Anzhou Xia,Zhi Xue,Tan Zhang,Tiantian Wei,Xingzhi Sha,Yixun Ding,Weidong Zhou 대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.1
To investigate the alteration of c-Jun N-terminal kinase (JNK) activity after myocardial ischemiareperfusion injury (MIRI) and further explore the effect of naloxone postconditioning on MIRI. Fortymale 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 visualizedby HE staining. The expression of p-JNK, and the apoptosis of cardiomyocytes were investigated withWestern blotting and the TUNEL assay, respectively. Irregular arrangement and aberrant structureof myocardial fibers, cardiomyocytes with granular or vacuolar degeneration, and inflammatory cellsinfiltrating the myocardial interstitial regions characterized MIRI in the IR group. Signs of myocardialinjury and inflammatory infiltration were less prominent in the Nal-treated groups. The expressionof p-JNK in the sham group and in all Nal-treated groups was significantly lower than that in theIR group (p<0.01). The apoptosis index of cardiomyocytes in the IR group was significantly higherthan in the sham group (p< 0.01). The apoptosis indices of cardiomyocytes in all Nal-treated groupswere significantly reduced to 55.4%, 26.2%, and 27.6%, respectively, of the IR group (p< 0.01). Thisstudy revealed that Naloxone postconditioning before reperfusion inhibits p-JNK expression anddecreases cell apoptosis, thus alleviating MIRI.