iNOS在大鼠创伤模型心肌细胞凋亡中的作用

 目的 观察iNOS在创伤大鼠模型心肌细胞凋亡中的作用。方法 用Noble-Collip创伤仪制备大鼠创伤模型，用Caspase-3活性和DNA ladder测定法观察心肌细胞凋亡，用Western blot测定心肌组织iNOS的蛋白表达，用化学发光法检测心肌组织一氧化氮（NO）的含量，ELISA法测定心肌组织硝基酪氨酸（NT）含量。结果 机械创伤后心肌细胞凋亡显著增加（P<0.01），心肌组织iNOS的表达显著升高（P<0.01），同时心肌组织NO2-/NO3-和NT含量明显增加（P<0.01）；给予iNOS选择性抑制剂1 400W可显著降低心肌细胞凋亡（P<0.05），且显著降低心肌组织NO2-/NO3-和NT的含量（NO2-/NO3-：P<0.01；NT：P<0.05）。结论 创伤时iNOS通过引起NO及过氧亚硝酸阴离子增加，进而导致心肌细胞凋亡。

The role of iNOS in cardiomyocyte apoptosis of rat trauma model

Objective To observe the role of iNOS in cardiomyocyte apoptosis of rat trauma model. Methods Trauma rats model was established by Noble-Collip drum. Cardiomyocyte apoptosis was determined by Caspase-3 activity and DNA ladder detection. The protein expression if iNOS was investigated by Western blot. Nitric oxide (NO) content in myocardial tissue was detected by chemiluminescene method. Myocardial nitrotyrosine (NT) content was measured by ELISA. Results Cardiomyocyte apoptosis was increased in mechanical trauma (P<0.01). Myocardial iNOS expression obviously increased after trauma (P<0.01). In addition, the product of NO2-/NO3- and NT, was elevated significantly in myocardial tissue after trauma (P<0.01). 1400W, a selective inhibition of iNOS, significantly decreased cardiomyocyte apoptosis(P<0.05), and the product of NO2-/NO3- and NT (NO2-/NO3-: P<0.01; NT: P<0.05). Conclusion iNOS caused cardiomyocyte apoptosis by increasing the levels of NO and peroxynitrite acid in myocardial tissue.