刺囊酸对缺氧复氧诱导心肌细胞凋亡相关基因表达的影响  

Effects of Echinocystic Acid on the Expression of Apoptosis-Associated Gene in the Rat Cardiomyocytes Subjected to Anoxia /Reoxygenation Injury

作　　者：陈杰[1] 沈映冰[2] 许静[3] 官碧琼[3] 罗子玲[3] 

机构地区：[1]中山大学附属第一医院药学部,广东省广州市510008 [2]中山大学附属第六医院药剂科,广东省广州市510655 [3]南方医科大学第三附属医院药剂科,广东省广州市510630

出　　处：《中国动脉硬化杂志》2013年第2期135-138,共4页Chinese Journal of Arteriosclerosis

基　　金：广东省自然科学基金(8451008901000788)

摘　　要：目的研究刺囊酸预处理对原代培养的SD乳鼠心肌细胞缺氧复氧损伤诱导的心肌细胞凋亡相关基因Bcl-2、Bax及聚二磷酸腺苷核糖聚合酶(PARP 89 kDa)表达的影响。方法实验随机分为6组:对照组,缺氧复氧损伤组,缺氧预处理组及低、中、高剂量刺囊酸组(0.5μmol/L、5μmol/L和50μmol/L),分别予以缺氧3 h后再复氧2 h,检测细胞存活率、乳酸脱氢酶(LDH)活性,Western Blot杂交法检测心肌细胞Bcl-2、Bax及PARP(89 kDa)蛋白表达变化。结果与对照组比较,缺氧复氧损伤组心肌细胞Bcl-2蛋白表达显著低于对照组(P<0.01),Bax蛋白及PARP(89 kDa)表达显著高于对照组(P<0.01),细胞存活率明显低于对照组(P<0.05)。与缺氧复氧损伤组比较,不同剂量的刺囊酸预处理能显著提高细胞存活率,降低LDH活性,呈剂量依赖性;中剂量刺囊酸显著增加Bcl-2蛋白表达(P<0.05),抑制Bax及PARP(89 kDa)蛋白表达(P<0.05)。结论刺囊酸预处理可通过上调Bcl-2蛋白表达,抑制PARP(89 kDa)及Bax蛋白表达,抑制细胞凋亡,对抗心肌细胞缺氧复氧损伤。Aim To study the effects of Echinocystic acid on the protein expression of apoptosis-associated Bcl-2, Bax and PARP （89 kDa） in the primary cultured rat cardiomyocytes subjected to anoxia/reoxygenation injury. Methods The cardiomyocytes were divided into normal group, anoxia/reoxygenation injury group, anoxia/reoxygenation preconditioning group, different concentration Echinocystic acid groups （0. 5 p.mol/L, 5 ~mol/L and 50 p^mol/L）. Car- diomyocytes were subjected to anoxia for 3 hours and subsequently reoxygenation for 2 hours. Cell viability and LDH activity in medium were measured. The expression o f Bcl-2 and the apoptotic protein Bax and PARP （89 kDa） were detected by Western Blot. Results Compared with that of the control group, the expression of Bcl-2 protein in cardiomyocytes decreased significantly （P 〈 0. 01 ） and the expression of Bax protein and PARP （89 kDa） in cardiomyocytes in- creased significantly （P 〈 0.011 ） after reoxygenation. Cell viability decreased obviously （ P 〈 0. 05 ）. Compared with that of the anoxia/reoxygenation group, pretreatment with different concentration Echinocystic acid decreased LDH activity and increased cell viability（P 〈0. 05）, the expression of Bcl-2 protein in the Echinocystic acid （5μmol/L） groups in- creased significantly （ P 〈 0. 05 ） and the expression of Bax protein decreased significantly （ P 〈 0.05 ）. Conclusion The antiapopotic effects of Echinocystic acid might be attributed to the up-regulated expression of Bcl-2 gene and the inhibited expression of Bax and PARP（89 kDa） gene expression.

关 键 词：刺囊酸 缺氧复氧损伤 心肌细胞 凋亡相关基因 

分 类 号：R96[医药卫生—药理学]