iNOS在大鼠创伤模型心肌细胞凋亡中的作用  

The role of iNOS in cardiomyocyte apoptosis of rat trauma model

作　　者：燕子[1,2] 郭丽[3] 杨丽红 高胜利[5] 王洁[1] 王瑾[1] 梁峰[6] 

机构地区：[1]山西医科大学基础医学院生理学系,山西太原030001 [2]山西医科大学细胞生理学省部共建教育部重点实验室,山西太原030001 [3]山西医科大学附属第二医院骨科实验室,山西太原030001 [4]山西医科大学基础医学院病理学教研室,山西太原030001 [5]山西医科大学汾阳学院生理学教研室,山西汾阳032200 [6]山西医科大学附属太钢总医院胸心外科,山西太原030003

出　　处：《基础医学与临床》2013年第6期675-679,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金(30872680);山西医科大学细胞生理学省部共建教育部重点实验室主任基金(2010-10)

摘　　要：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1 400 W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。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 easpase-3 activity and DNA ladder detection. The protein expression of iNOS was investigated by Western blot. Nitric oxide （NO） content in myocardial tissue was detected by chemiluminescene method. Myocardial nitrotyrosine（NT） con tent 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, significantly elevated in myocardial tissue after trauma（P 〈 0.01 ）. 1 400 W, a selective inhibition of iNOS, significantly decreased eardiomyocyte apoptosis （P 〈 0. 05 ）, and the product of NO2 -/NO3 - and NT （NO2 -/NO3 - ： P 〈 0. 01 ; NT： P 〈 0. 05 ）. Conclusions iNOS caused cardiomyocytc apoptosis by increasing thelevels of NO and peroxynitrite acid in myocardial tissue.

关 键 词：心脏损伤 一氧化氮合酶 一氧化氮 过氧亚硝酸阴离子 凋亡 

分 类 号：R641[医药卫生—外科学]