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目的:探讨重组人脑利钠肽(rhBNP)后适应对兔急性缺血/再灌注(I/R)心肌的保护作用及其机制。方法:将36只健康日本大耳白兔随机分为3组(每组12只)。即假手术组、I/R组(缺血40 min后再灌注180 min)及BNP+I/R组(I/R前5 min以0.01μg/kg静脉给予BNP)。假手术组开胸于左室支下穿线但不结扎,观察180 min结束;I/R组及BNP+I/R组:缺血40 min,分别再灌注180 min后处死。进行心肌酶学CK-MB含量检测,观察心肌HE染色后病理形态变化及BCI-2、Bax表达的检测。结果:与假手术组相比,I/R组和BNP+I/R组CK-MB的水平均显著增高(P<0.01)。与I/R组相比,BNP+I/R组明显减少这些心肌酶的升高(P<0.01)。与假手术组相比,I/R组及BNP+I/R组均可见到凋亡细胞,但BNP+I/R组凋亡细胞明显减少。与假手术组相比,I/R组Bax的表达增加,Bcl-2的表达降低。与I/R组相比,BNP+I/R组Bax的表达明显降低,而Bcl-2的表达明显升高。结论:重组人脑钠尿肽可减少梗死后心肌的损伤;可以增加梗死后心肌细胞抑制凋亡基因(Bcl-2)的表达,从而减少心肌细胞的凋亡。
Objective: To investigate the protective effect of recombinant human brain natriuretic peptide (rhBNP) on acute myocardial ischemia / reperfusion (I / R) myocardium and its mechanism. Methods: 36 healthy Japanese white rabbits were randomly divided into 3 groups (12 in each group). I / R group (180 min reperfusion after 40 min ischemia) and BNP + I / R group (BNP was intravenously administrated at 0.01 μg / kg 5 min before I / R). Sham-operated group was thoracotomy on the left ventricular branch but not ligated, and observed the end of 180 min; I / R group and BNP + I / R group: ischemia 40 min, were reperfused 180 min before sacrifice. CK-MB was detected by enzyme-linked immunosorbent assay (ELISA). The pathological changes of myocardium and the expression of BCI-2 and Bax were observed. Results: The levels of CK-MB in I / R group and BNP + I / R group were significantly higher than those in sham operation group (P <0.01). Compared with I / R group, BNP + I / R group significantly reduced these myocardial enzymes (P <0.01). Compared with sham operation group, apoptotic cells were found in I / R group and BNP + I / R group, but apoptotic cells in BNP + I / R group were significantly decreased. Compared with the sham operation group, the expression of Bax increased and the expression of Bcl-2 decreased in I / R group. Compared with I / R group, the expression of Bax in BNP + I / R group was significantly decreased, while the expression of Bcl-2 was significantly increased. Conclusion: Recombinant human natriuretic peptide can reduce the myocardial injury after infarction. It can increase the expression of Bcl-2 and decrease the apoptosis of cardiomyocytes after myocardial infarction.