雌激素膜受体GPR30对NE诱导的新生大鼠心肌细胞肥大作用的实验研究  

Experimental Study of the Effect of Membranous Estrogen Receptor GPR30 on the Norepinephrine-induced Myocardial Cell Enlargement of Newborn Mice

作　　者：卢佳佳[1] 陈文生[1] 赵堃[1] 李子林[1] 杨建宝[1] 杨阳[1] 陈涛[1] 

机构地区：[1]第四军医大学西京医院心血管外科,陕西西安710032

出　　处：《临床医学工程》2011年第2期173-175,共3页Clinical Medicine & Engineering

基　　金：陕西省自然科学基金资助(2007C224)

摘　　要：目的探讨雌激素膜受体GPR30对去甲肾上腺素(NE)诱导的新生大鼠心肌细胞肥大的作用。方法培养的新生大鼠心肌细胞分为空白对照组、NE诱导的心肌细胞肥大组(模型组)和在模型组的基础上应用不同浓度GPR30特异性激动剂(G-1)处理的实验组,G-1的浓度分别为10pmol/L、100pmol/L、1nmol/L、10nmol/L。应用免疫荧光细胞化学技术检测GPR30在心肌细胞内的表达、MTT和PI-hoechst染色对各组心肌细胞增值凋亡情况进行分析。结果 GPR30在心肌细胞内大量表达,属于胞膜受体;它可抑制NE诱导心肌细胞的肥大,且具有浓度依赖性。结论 GPR30可抑制去甲肾上腺素所诱导的心肌细胞肥大。Objective To explore the effect of membranous estrogen receptor GPR30 on the norepinephrine-induced myocardial cell enlargement of newborn mice. Methods Myocardial cells of newborn mice were cultured and then divided into control group, myocardial cell enlargement group （model group） and the groups with GPR30 agonist probe G-1 treatment based on the model. G-lconcentration was 10 pmol/L, 100 pmol/L, 1 nmol/L and 10 nmol/L, respectively. The expression of GPR30 in the myocardial cells of newborn mice was detected by immunofluorescence technique. Their profiferation and apoptosis were analyzed after MTT and PI-hoechst dying. Results GPR30 was a membranous receptor and expressed in a massive manner. It could inhibit the norepinephrine-induced myocardial cell enlargement of new born mice in the concentration-dependent manner. Conclusion GPR30 can inhibit the norepinephrine-induced myocardial cell enlargement of newborn mice.

关 键 词：GPR30 G-1 去甲肾上腺素 心肌细胞肥大 

分 类 号：R541[医药卫生—心血管疾病]