摘要
目的 探讨PGE1对缺氧复氧乳鼠心肌细胞凋亡的影响及其作用机制。方法 用原代培养的乳鼠心肌细胞建立缺氧 3 0min复氧 40min损伤模型 ,DNA琼脂糖凝胶电泳和原位末端标记技术 (TUNEL)检测缺氧复氧乳鼠心肌细胞的凋亡 ,原位杂交法检测bcl 2、baxmRNA的含量。结果 模型组乳鼠心肌细胞DNA琼脂糖凝胶电泳呈明显的梯状图谱 ,TUNEL法检测到较多的阳性标记 ,PGE1各给药组随剂量的增加 ,电泳中的DNA梯状条带逐渐减弱 ,PGE1(0 12 7μmol·L- 1)组心肌细胞的凋亡率 (6 80 %± 1 99% )与模型组 (11 40 %± 2 3 2 % )相比差异有统计学意义 (P <0 0 1) ;模型组与正常组相比bcl 2mRNA的含量下降、baxmRNA的含量增加 ,PGE1各给药组与模型组相比能明显的上调bcl 2mRNA的含量、下调baxmRNA的含量。结论 离体培养的乳鼠心肌细胞建立的缺氧复氧损伤模型可诱导心肌细胞的凋亡。PGE1可明显抑制这种凋亡的发生 ,其机制可能与促进bcl 2mRNA的表达。
AIMTo investigate the effects of prostaglandin E 1 on apoptosis induced by hypoxia/reoxygenation in cultured neonatal rat cardiomyocy tes. METHODSThe models of hypoxia/reoxygenation were made with t he first generation of cultured cardiomyocytes. Hypoxia/reoxygenation apoptosis in cultured neonatal rat cardiomyocytes was studied by agarose gel electrophores is and Tdt-mediated dUTP nick end labeling(TUNEL). Bcl-2 and bax mRNA were det ected by in situ hybridization. RESULTSThe results of DNA electr ophoresis in the H/R group showed the typical DNA ladder. And the DNA ladder decreased gradually corresponding to the increased dose of PGE 1. The TUNEL staining showed that the total number of apo ptotic cells in the H/R group was much biger than that in PGE 1(0 127 μmol·L -1 ) group. The results of in situ hybridization showed that the conten t of bcl-2 mRNA in H/R group was lower than control. And the content of bax mRN A showed a reverse result as bcl-2 mRNA. Compared with H/R group, the content o f bcl-2 mRNA was significantly higher after treatment with PGE 1(0 014 μmol ·L -1 , 0 042 μmol·L -1 , 0 127 μmol·L -1 ). But the content of bax mRNA in PGE 1(0 014 μmol·L -1 , 0 042 μmol·L -1 , 0 127 μmol·L -1 )groups was significantly lower than H/R group. CONCLUSI ONH/R injury can induce cardiomyocyte apoptosis. PGE 1 has obvious an ti-apoptotic effects on cardiomyocyte and the mechanisms are possibly by inhibi ting the expression of bax and increasing the expression of bcl-2.hein
creaseddoseofPGE1 .TheTUNELstainingshowed
thatthetotalnumberofapoptoticcellsintheH
出处
《中国药理学通报》
CAS
CSCD
北大核心
2004年第3期303-307,共5页
Chinese Pharmacological Bulletin
