c-jun反义基因转染对缺氧复合烧伤血清处理心肌细胞保护作用的分子机制研究

Molecular Mechanism of c-jun Antisense Gene Transfection in Protecting Cardiomyocyte from Injury of Hypoxia and Burn Serum Treatment

目的 探讨c -jun反义基因转染对缺氧复合烧伤血清处理心肌细胞保护作用的分子机制。方法 烧伤血清采自3 0 %TBSAⅢ度烫伤Wistar大鼠 ;采用含 1%O2 的混和气体作为缺氧模型 ;采用基因重组技术构建c -jun反义基因重组体 ;由Lipo fectaminekit介导心肌细胞转染 ;缺氧复合烧伤血清处理后 12、2 4和 48h不同时相点采用Westernblot检测c -jun蛋白 ,PKCα和JNK的表达变化。结果 加入烧伤血清并造成缺氧的非转染心肌细胞 (非转染组 ) ,c -jun蛋白 ,PKCα和JNK均显著表达 ,2 4h达最高峰 ;转染c -jun反义基因重组体 (转染组 )后 ,c -jun蛋白 ,PKCα和JNK表达均明显下降。结论 c

Objective To explore the molecular mechanism of c-jun antisense gene transfection in protecting cardiomyocytes from injury of hypoxia and burn serum treatment. Methods Burn sera were collected from wistar rat with 30% total body surface area(TBSA) Ⅲ degree burn injury, and the mixture gas containning 1% O 2 was used as hypoxia model. The c-jun antisense gene recombinant vector was constructed. Neonatal wistar rat cardiomyocytes cultured in vitro were treated with hypoxia and burn sera. c-jun antisense gene recombinant vector was transfected into the cultured cardiomyocytes. Expressions of c-jun, PKCα and JNK were detected with western blot in the transfected and non-transfected cardiomyocytes. Results Expression levels of c-jun, PKCα and JNK significantly increased in the non-transfected cardiomyocytes when treated by hypoxia and burn sera, up to maximum 24 hour after the treatment. Expression levels of c-jun, PKCα and JNK in the transfected cardiomyocytes decreased significantly compared with non-transfected cells. Conclusions The transfection of the c-jun antisense gene recombinant vector protected cardiomyocytes from injury of hypoxia and burn sera treatment via down-regulating PKCα and JNK expressions.