摘要
目的观察血管紧张素(1-7)对心肌肥厚内质网应激所致细胞损伤的保护作用。方法实验分为空白对照组、血管紧张素Ⅱ组、血管紧张素(1-7)干预组。体外培养乳鼠心肌细胞,用不同浓度血管紧张素Ⅱ(100 nmol/L、1000 nmol/L)分别作用24 h、48 h、72 h诱导其肥厚。用不同浓度的血管紧张素(1-7)(10 nmol/L、100 nmol/L、1000 nmol/L)进行干预。实验终止后,在倒置相差显微镜下观察心肌细胞形态变化。考马斯亮蓝G-250法测定心肌总蛋白合成。RT-PCR和W estern B lotting检测内质网应激相关分子葡萄糖调节蛋白78和C/EBP同源蛋白的表达。结果与空白对照组相比,100 nmol/L血管紧张素Ⅱ干预24 h可诱导心肌肥厚,心肌细胞体积增大,细胞蛋白含量增加(1.59±0.03 g/L,P<0.05),葡萄糖调节蛋白78和C/EBP同源蛋白mRNA和蛋白表达水平明显增高(P<0.05),给予血管紧张素(1-7)干预后,可较大程度地逆转上述指标变化(P<0.05)。结论血管紧张素Ⅱ诱导的心肌细胞肥厚存在内质网应激。血管紧张素(1-7)可以通过减轻内质网应激来减轻心肌细胞肥厚,对心肌细胞具有保护作用且1000 nmol/L血管紧张素(1-7)的保护作用最强。
Aim To observe effect of angiotensin（1-7）（Ang-1-7） on myocardial hypertrophy in endoplasmic reticulum stress（ERS） induced cell injury. Methods Experiment was divided into control group,angiotensin Ⅱ（AngⅡ） group,AngⅡ ＋ Ang-1-7 group.Cultured rat myocardial cells were induced hypertrophy by different concentrations of AngⅡ（100 nmol / L,1000 nmol / L） for 24,48 and 72 hours,and intervened by different concentrations of Ang-1-7（10 nmol/L,100 nmol/L,1000 nmol/L）.After finishing experiment,the change of myocardial cells was observed in an inverted phase contrast microscope.Coomassie brilliant blue G-250 was used to determine cardiac total protein synthesis.Reverse transcription polymerase chain reaction（RT-PCR） and Western-Blotting were used to detect glucose-regulated protein 78（GRP78） and C/EBP homologous protein（CHOP） expression of endoplasmic reticulum stress（ERS）. Results Compared with the control group,100 nmol/L AngⅡ induced cardiac hypertrophy at 24 h,the myocardial cell volume increased,the cell protein content increased（1.59±0.03 g/L,P0.05）.mRNA and protein expression levels of endoplasmic reticulum stress proteins GRP78 and CHOP were significantly higher（P0.05）;Ang-1-7 can reverse the above to a large extent（P0.05）. Conclusion Myocardial hypertrophy induced by AngⅡ exist endoplasmic reticulum stress.Ang-1-7 can reduce the endoplasmic reticulum stress by reducing cardiac hypertrophy,and protect myocardial cells;Protective effect of 1000 nmol/L Ang-1-7 was the strongest.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2011年第1期44-48,共5页
Chinese Journal of Arteriosclerosis
