摘要
目的探讨反应性氧族(ROS)在致心肌细胞肥大时同时促进心肌细胞分泌内皮素的作用。方法在原代培养的乳鼠心肌细胞中。细胞内的氧活性产物用ROS敏感的荧光探针2,7-dichlorofluores-cindictate(DCF-DA)检测。用RT-PCR的方法检测内皮素基因的表达。结果空白对照组细胞内发现极少量氧活性产物的生成,内皮素-1基因仅少量表达;加用抗氧化剂N-乙酰半胱氨酸(N-acetylcysteine)的实验组内仅有极少量氧活性产物,和对照组相比细胞内DCF-DA荧光强度:N-乙酰半胱氨酸加用ET-1组增加4.8%,N-乙酰半胱氨酸加用AngⅡ组增加3.0%;内皮素-1基因的表达与空白对照组没有明显差异,Prepro-ET相对量增加依次为:N-乙酰半胱氨酸加用ET-1组增加3.8%,N-乙酰半胱氨酸加用AngⅡ组增加2.9%。单用ET-1及AngⅡ组均见到大量氧活性产物,细胞内DCF-DA荧光强度增加依次为108.8%,104.9%;内皮素-1基因的表达也明显增强,Prepro-ET相对量增加依次为52.4%,51.1%。结论ROS在缩血管因子致心肌心细胞的肥大过程中起到信号传递作用,同时ROS也增强内皮素-1基因在心肌细胞的表达。
Objective To explore role of ROS in hypertrophic cardiomyocytes induced by the vaso- constrictors such as ET-1, Ang Ⅱ etc. Methods Neonatal cardiac myocytes were cultured and stimulated by ET-1 and Ang Ⅱ. Antioxidant N-acetylcysteine was used to block the intracellular synthesis of ROS. 2,7-dichlorofluorescin dictate was used to examine the intracellular ROS. We examined the expression of preproendothelin-1 gene by RT-PCR assay. Results We found that N-acetylcysteine pronouncedly block the synthesis of ROS and the expression of endothelin-1 gene. Compared with the control group, the fluorescence intensity of intercellular DCF-DA is increased in N-acetylcysteine and Ang 1I group（ ＋4. 6%, N-acetylcysteine and ET-1 group （ ＋ 4. 8 % ）, ET-1 alone （ ＋ 108. 8 % ） and Ang Ⅱ alone （ ＋ 104. 9 % ）. The expression of Prepro ET-1 increased by 3.8 %, 2.9%, 52.4%, 51.1% correspondingly. Conclusion It indicates that ROS is pivotal in vasoconstrictor-induced cardiomyocyte hypertrophy, which was associated with increases in endothelin-1 gene expression in cardiomyocytes.
出处
《高血压杂志》
CAS
CSCD
北大核心
2005年第10期624-627,共4页
Chinese Journal of Hypertension
