睾酮对血管紧张素Ⅱ诱导的乳鼠心肌成纤维细胞增殖和胶原合成的影响  

Effect of testosterone on proliferation and collagen synthesis of neonatal rat cardiac fibroblast induced by angiotensinⅡ

作　　者：孙丽娜[1] 王颖[1] 燕树勋[2] 张彦周[3] 魏子涵[1] 秦鹏[1] 孙素珂 

机构地区：[1]郑州大学第一附属医院老年医学科,郑州450052 [2]河南中医学院第一附属医院内分泌科,郑州450008 [3]郑州大学第一附属医院心内科,郑州450052 [4]河南省高等学校临床医学重点学科开放实验室,郑州450052

出　　处：《郑州大学学报（医学版）》2014年第4期461-464,共4页Journal of Zhengzhou University(Medical Sciences)

基　　金：河南省教育厅科学技术研究重点项目(基础研究计划)13A320436;河南省医学科技攻关计划项目2011020038;河南省卫生科技创新型人才工程中青年科技人才项目4099;河南省科技厅河南省基础与前沿科技研究计划项目;郑州大学第一附属医院青年创新基金

摘　　要：目的:观察睾酮对血管紧张素Ⅱ(AngⅡ)诱导的乳鼠心肌成纤维细胞(CF)增殖和胶原合成的影响。方法:分离、培养CF,分别用无血清DMEM培养液(对照组)、含10-6mol/L AngⅡ的无血清DMEM培养液(AngⅡ组)、含30 nmol/L睾酮的无血清DMEM培养液(睾酮组)、含30 nmol/L睾酮和10-6mol/L AngⅡ的无血清DMEM培养液(睾酮+AngⅡ组)培养24 h,应用流式细胞技术检测细胞周期分布,VG染色法检测胶原含量,免疫细胞化学染色法检测磷酸化ERK1/2(p-ERK1/2)的表达。结果:AngⅡ组S期细胞比例、胶原含量和p-ERK1/2表达水平较对照组和睾酮组明显增加,睾酮+AngⅡ组S期细胞比例、胶原含量和p-ERK1/2表达水平较AngⅡ组明显降低(S期细胞比例:FAngⅡ=30.403,F睾酮=5.812,F交互=18.073,P<0.05;胶原含量:FAngⅡ=10.365,F睾酮=4.533,F交互=42.049,P<0.05;p-ERK1/2表达水平:FAngⅡ=174.762,F睾酮=184.828,F交互=152.240,P<0.05)。结论:睾酮可能通过抑制ERK1/2的活化,抑制AngⅡ诱导的CF的增殖和胶原合成。Aim： To explore the effect and the mechanism of testosterone on proliferation and collagen synthesis of neonatal rat cardiac fibroblast（ CF） induced by angiotensinⅡ（ AngⅡ）. Methods： CFs derived from the neonatal rat were cultured with serum-free DMEM culture（ control group）,10- 6mol /L Ang Ⅱ（ Ang Ⅱ group）,30 nmol /L testosterone（ testosterone group）,or 30 nmol/L testosterone and 10- 6mol /L Ang Ⅱ（ testosterone ＋ Ang Ⅱ group） for 24 h,respectively. Flow cytometry technique was used to detect the cell cycle distribution. VG staining method was used to detect the contents of collagen,and immunocytochemistry method was used to detect phosphorylated ERK1 /2（ p-ERK1 /2） expression. Results： S phase cells proportion,collagen content and p-ERK1 /2 expression level of AngⅡ group were significantly higher than those of the control group and testosterone group,and these indexes of testosterone ＋ AngⅡ group were lower than those of AngⅡgroup（ S phase cells proportion： FAngⅡ= 30. 403,Ftestosterone= 5. 812,Finteraction= 18. 073,P〈0.05; collagen content： FAngⅡ= 10. 365,Ftestosterone= 4. 533,Finteraction= 42. 049,P〈0.05; p-ERK1 /2 expression level： FAngⅡ= 174. 762,Ftestosterone=184. 828,Finteraction= 152. 240,P〈0.05）. Conclusion： Testosterone can inhibit CF proliferation and collagen synthesis induced by AngⅡ,and the mechanism may be related to the inhibition of ERK1 /2 activation.

关 键 词：睾酮 血管紧张素Ⅱ 心肌成纤维细胞 增殖 胶原 ERK1 2 乳鼠 

分 类 号：R542.2[医药卫生—心血管疾病]