三碘甲状腺原氨酸对缺血再灌注损伤后未成熟心肌细胞中Bax、Bcl-2的影响  

The Effects of Triiodothyronine on the Bax and Bcl-2 of Immature Cadiocytes while Given Ischemical Reperfusion Injury

作　　者：雷伟程[1] 徐建军[1] 

机构地区：[1]南昌大学第二附属医院心胸外科,江西省南昌市330006

出　　处：《中国动脉硬化杂志》2011年第8期665-667,共3页Chinese Journal of Arteriosclerosis

摘　　要：目的通过三碘甲状腺原氨酸对缺血再灌注损伤后未成熟心肌细胞中Bax、Bcl-2表达的影响,探讨其作用机制。方法培养原代乳鼠未成熟心肌细胞,通过缺氧复氧建立乳鼠心肌细胞缺血再灌注模型。于缺氧复氧前期给予三碘甲状腺原氨酸处理,通过聚合酶链反应仪检测三碘甲状腺原氨酸干预后心肌细胞的Bax mRNA和Bcl-2 mRNA表达情况。结果缺氧复氧前短期给予三碘甲状腺原氨酸可下调乳鼠未成熟心肌细胞Bax的表达,上调Bcl-2的表达,减少心肌细胞凋亡。结论三碘甲状腺原氨酸可以提高未成熟心肌抗缺血再灌注损伤的能力,而对心肌细胞凋亡这种保护作用与心肌细胞Bcl-2和Bax的表达相关。Aim To study the effects of triiodothyronine on the Bax and Bcl-2 of immature cadiocytes while given ischemical reperfusion injury. Methods The cadiocytes of neonate rat were culrured in vitro,and the ischemical reperfusion injury of cadiocytes were induced by anoxia-reoxygenation.Triiodothyronine（T3） was administered before anoxia-reoxygenation at a concentration of 1 μg/L,Bcl-2 mRNA and Bax mRNA were detected by polymerase chain reaction（PCR）. Results The Bcl-2 were down-regulated and Bax were up-regulated while given T3 shortly before anoxia-reoxygenation.At the same time,the apoptosis of cadiocytes were reduced. Conclusions Giving triiodothyronine before anoxia-reoxygenation would enhance the ablity of immature cadiocytes against ischemical reperfusion injury,and could reduce the apoptosis of cadiocytes.This effect was associated with the expression of Bcl-2 and Bax.

关 键 词：三碘甲状腺原氨酸 缺氧复氧 BCL-2/BAX 

分 类 号：R363[医药卫生—病理学]