CAJ | 학술논문

目的评价氨基胍对大鼠急性心肌缺血时细胞凋亡的影响.方法健康成年雄性SD大鼠30只,体重250 ～ 290 g,采用随机数字表法分为3组(n=10):假手术组(S组)、心肌缺血损伤组(Ⅰ组)和氨基胍组(AG组).采用结扎大鼠左冠状动脉前降支的方法,制备急性心肌缺血损伤模型.AG组于缺血6h时腹腔注射氨基胍100 mg/kg,Ⅰ组给予等容量生理盐水.于氨基胍给药后3h开胸取心脏.采用TUNEL法测定心肌细胞凋亡率,采用免疫组化法测定心肌细胞Bcl-2和Bax蛋白的表达,并计算Bcl-2/Bax比值;光镜下观察心肌组织病理学结果.结果与S组比较,Ⅰ组心肌细胞凋亡率升高,Bax蛋白表达上调,Bcl-2蛋白表达下调,Bcl-2/Bax比值降低(P＜0.01);与Ⅰ组比较,AG组心肌细胞凋亡率降低,Bax蛋白表达下调,Bcl-2蛋白表达上调,Bcl-2/Bax比值升高(P＜0.01).AG组心肌病理学损伤程度较Ⅰ组减轻.结论氨基胍可抑制心肌细胞凋亡,有助于减轻大鼠急性心肌缺血损伤.
목적 평개안기고대대서급성심기결혈시세포조망적영향.방법 건강성년웅성SD대서30지,체중250 ～ 290 g,채용수궤수자표법분위3조(n=10):가수술조(S조)、심기결혈손상조(Ⅰ조)화안기고조(AG조).채용결찰대서좌관상동맥전강지적방법,제비급성심기결혈손상모형.AG조우결혈6h시복강주사안기고100 mg/kg,Ⅰ조급여등용량생리염수.우안기고급약후3h개흉취심장.채용TUNEL법측정심기세포조망솔,채용면역조화법측정심기세포Bcl-2화Bax단백적표체,병계산Bcl-2/Bax비치;광경하관찰심기조직병이학결과.결과 여S조비교,Ⅰ조심기세포조망솔승고,Bax단백표체상조,Bcl-2단백표체하조,Bcl-2/Bax비치강저(P＜0.01);여Ⅰ조비교,AG조심기세포조망솔강저,Bax단백표체하조,Bcl-2단백표체상조,Bcl-2/Bax비치승고(P＜0.01).AG조심기병이학손상정도교Ⅰ조감경.결론 안기고가억제심기세포조망,유조우감경대서급성심기결혈손상.
Objective To evaluate the effect of aminoguanidine on cell apoptosis induced by acute myocardial ischemia in rats.Methods Thirty adult male Sprague-Dawley rats,weighing 250-290 g,were randomly divided into 3 groups (n =10 each):sham operation group (group S),myocardial ischemia group (group Ⅰ),and aminoguanidine group (group AG).The model of acute myocardial ischemia was established by ligating the left anterior descending branch of the coronary artery of rats anesthetized with chloral hydrate.Aminoguanidine 100 mg/kg was intraperitoneally administrated at 6 h of ischemia in AG group,while the equal volume of normal saline was given instead of aminoguanidine in group Ⅰ.The chest was opened at 3 h after aminoguanidine administration and hearts were quickly removed for detection of apoptosis in cardiomyocytes (by TUNEL) and expression of Bcl-2 and Bax in cardiomyocytes (by immuno-histochemistry),and for microscopic examination with light microscope.Apoptotic rate was calculated.Results Compared with group S,the apoptotic rate was significantly increased,the expression of Bax was up-regulated,and the expression of Bcl-2 was downregulated and the ratio of Bcl-2/Bax was decreased in group Ⅰ.Compared with group Ⅰ,the apoptotic rate was significantly decreased,the expression of Bax was down-regulated,and the expression of Bcl-2 was up-regulated,and the ratio of Bcl-2/Bax was increased in group AG.The pathological changes of myocardial cells were significantly attenuated in AG group as compared with group Ⅰ.Conclusion Amionguanidine can inhibit apoptosis in cardiomyocytes and is helpful in mitigating injury induced by acute myocardial ischemia in rats.