Effect of Brain-derived Neurotrophic Factor Pretreatment for Reducing Myocardial Ischemia/reperfusion Injury in Experimental Rats
10.3969/j.issn.1000-3614.2016.02.017
- VernacularTitle:脑源性神经营养因子预处理减轻大鼠心肌缺血再灌注损伤
- Author:
Mingyi LV
;
Shuling DENG
;
Xiaofeng LONG
- Publication Type:Journal Article
- Keywords:
Neurturin;
Myocardial reperfusion injury;
Ischemic pretreatment
- From:
Chinese Circulation Journal
2016;31(2):175-179
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect and mechanism of brain-derived neurotrophic factor (BDNF) pretreatment for reducing myocardial ischemia/reperfusion (I/R) injury in experiment rats.
Methods: Rat’s myocardial I/R model was established by left anterior descending artery ligation for 30min followed-by reperfusion for 180 min. The rats were divided into 5 groups:Sham operation group, I/R group and IR with BDNF pretreatment (1, 10, 100) nmol/(kg·ml) groups respectively. The LVSP, LVEDP, ±dp/dtmax were recorded after I/R;serum levels of LDH, CK and the cardiac tissue levels of MDA, SOD were examined;the ratios of left ventricular myocardial infarction area in different groups were observed by by Evans blue staining;cell apoptosis rates were evaluated by Tunel staining;the total-TrkB and p-TrkB in myocardium were detected by Western-blot analysis.
Result: Compared with I/R group, in 3 IR with BDNF pretreatment groups, LVSP, ±dp/dtmax were gradually increasing and LVEDP were gradually decreasing, all P<0.05;the leaking levels of LDH, CK and the content of MDA were gradually decreasing and the SOD activity was gradually increasing, all P<0.05;the average ratios of MI area/ischemic area were decreased from (47.54 ± 6.35)%to (28.68 ± 4.56)%, the apoptosis rates decreased from (37.89 ± 5.46)%to (10.24 ± 3.05)%, the level of p-trkB/Total-TrkB increased from (0.16 ± 0.03) to (0.42 ± 0.03), P<0.05.
Conclusion: BDNF pretreatment could maintain the cardiac function in experiment rats after I/R injury, it may reduce MI area, decrease oxidative damage and apoptosis, therefore, protect myocardial cells for reducing IR injury.
