CAJ | 학술논문

目的通过建立在体大鼠心肌缺血再灌注模型,探讨脑利钠肽预处理对在体大鼠心肌缺血再灌注损伤心肌细胞凋亡及对凋亡基因bcl-2、Bax表达的影响.方法 21只雄性SD大鼠,随机数字表法分为3组:(1)假手术组:只开胸,不结扎冠状动脉;(2)缺血再灌注组:结扎冠状动脉左前降支35 min、再灌注4 h;(3)脑利钠肽(BNP)组:缺血前10 min,静脉开始予以BNP 0.01μg·kg-1·min-1,结扎冠状动脉左前降支35 min,再灌注4 h,BNP静脉恒速维持至再灌注结束.用TUNEL法检测缺血再灌注心肌细胞的凋亡,用反转录聚合酶链反应、Western印迹方法检测缺血再灌注心肌bcl-2和Bax的表达.结果假手术组、BNP组与缺血再灌注组的心肌细胞凋亡指数分别为5.4%±4.2%、22.5%±9.5%、45.2%±13.0%(P＜0.05).bcl-2蛋白表达假手术组、BNP组明显高于缺血再灌注组,分别为0.87±0.09、0.70±0.07、0.38±0.09(P＜0.05);假手术组、BNP组与缺血再灌注组的Bax蛋白表达分别为0.08±0.04、0.39±0.09、0.71±0.18(P＜0.01).假手术组、BNP组、缺血再灌注组的bcl-2/Bax比值分别为0.763±0.154、0.099±0.025、0.022±0.024(P＜0.05).结论 BNP预处理能减少心肌缺血再灌注损伤导致的心肌细胞凋亡,其机制可能与其增加bcl-2表达、抑制Bax表达,从而上调bcl-2/Bax比值相关.
목적 통과건립재체대서심기결혈재관주모형,탐토뇌리납태예처리대재체대서심기결혈재관주손상심기세포조망급대조망기인bcl-2、Bax표체적영향.방법 21지웅성SD대서,수궤수자표법분위3조:(1)가수술조:지개흉,불결찰관상동맥;(2)결혈재관주조:결찰관상동맥좌전강지35 min、재관주4 h;(3)뇌리납태(BNP)조:결혈전10 min,정맥개시여이BNP 0.01μg·kg-1·min-1,결찰관상동맥좌전강지35 min,재관주4 h,BNP정맥항속유지지재관주결속.용TUNEL법검측결혈재관주심기세포적조망,용반전록취합매련반응、Western인적방법 검측결혈재관주심기bcl-2화Bax적표체.결과 가수술조、BNP조여결혈재관주조적심기세포조망지수분별위5.4%±4.2%、22.5%±9.5%、45.2%±13.0%(P＜0.05).bcl-2단백표체가수술조、BNP조명현고우결혈재관주조,분별위0.87±0.09、0.70±0.07、0.38±0.09(P＜0.05);가수술조、BNP조여결혈재관주조적Bax단백표체분별위0.08±0.04、0.39±0.09、0.71±0.18(P＜0.01).가수술조、BNP조、결혈재관주조적bcl-2/Bax비치분별위0.763±0.154、0.099±0.025、0.022±0.024(P＜0.05).결론 BNP예처리능감소심기결혈재관주손상도치적심기세포조망,기궤제가능여기증가bcl-2표체、억제Bax표체,종이상조bcl-2/Bax비치상관.
Objective To study the effects of B-type natriuretic peptide (BNP) preconditioning on the apoptosis and expressions of bcl-2 and Bax in rat cardiomyocytes during myocardial ischemia-reperfusion.Methods Twenty-one male Sprague-Dawley rats weighing (250 ± 50) g were randomly divided into 3 groups of sham operation ( SHAM ), ischemia-reperfusion (I/R) and B-type natriuretic peptide ( BNP). A rat model of in vivo myocardial ischemia-reperfusion injury was established by ligating the left anterior descending coronary artery for 35 minutes and then reperfusing for 240 minutes. The apoptosis of myocardial cell was determined by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end-labeling (TUNEL) method. Real-time polymerase chain reaction and Western blot were used to detect the expression changes of bcl-2 and Bax in rat ischemia myocardium. Results The apoptotic indices of SHAM, BNP and L/R groups were 5.4% ±4.2%, 22.5% ±9.5% and 45.2% ±13.0% respectively (P＜0.05). The bcl2 protein expression of SHAM, BNP and I/R groups were 0. 87 ± 0. 09, 0. 70 ± 0. 07 and 0. 38 ± 0. 09respectively ( P ＜ 0. 05). The Bax protein expression of SHAM, BNP and I/R groups were 0.08 ± 0. 04,0. 39 ±0. 09 and 0. 71 ± 0. 18 respectively ( P ＜0. 01 ). The bcl-2/Bax mRNA ratio of SHAN, BNP and I/R groups were 0. 763 ± 0. 154, 0. 099 ± 0. 025 and 0. 022 ± 0. 024 respectively ( P ＜ 0. 05 ). Conclusion The BNP preconditioning can decrease the myocardial apoptosis induced by ischemia-reperfusion injury. The mechanisms may be associated with an elevated expression of bcl-2, an increased ratio of bcl-2/Bax and a lowered expression of Bax.