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血管活性肽和生长因子是性质不同且胞浆头端信号通路各异的两种具有丝裂原活性的物质。本文研究丝裂原活化蛋白激酶(MAPK) 在血管紧张素Ⅱ(Ang Ⅱ) 和表皮生长因子(EGF) 诱导的心肌成纤维细胞(FB) 分裂反应中的作用及反义MAPK 寡核苷酸的抗分裂作用和机制。结果如下:(1)Ang Ⅱ或EGF( 浓度均为10- 8 mol/L) 处理培养新生大鼠FB24 h,FB数增加39 % 和68 % , DNA 合成速率(3Hthymidine 掺入法) 增加60 % 和102 % ;(2)FB 经Ang Ⅱ(5min) 或EGF(10 min) 处理后, MAPK活性(γ32P掺入法) 分别增加202 % 和305 % ; 磷酸化MAPK蛋白含量( 免疫印迹法) 增加545 % 和646 % ;(3) 脂质体转染法将反义MAPK 寡脱氧核苷酸(ODN) 导入FB, MAPK 蛋白表达显著被抑制;AngⅡ或EGF诱导的FBDNA合成速率比脂质体对照组分别降低58 % 和46 % , 细胞数降低38 % 和44% ; 磷酸化MAPK含量降低85 % 和90 % ,MAPK活性降低74-2% 和65-9% 。结果提示, 在Ang Ⅱ或EGF诱导的心肌FB分裂反应中均有MAP?
Vasoactive peptides and growth factors are two mitogen-active substances with different properties and different cytoplasmic head-end signaling pathways. This article studies the role of mitogen-activated protein kinase (MAPK) in the cardiomyocyte fibroblast (FB) -fibroblast response induced by angiotensin II (Ang II) and epidermal growth factor (EGF) and the effect of antisense MAPK oligonucleotide Anti-division and mechanism. The results were as follows: (1) The FB number increased by 39% and 68%, the DNA synthesis rate (3Hthymidine incorporation method) increased with the treatment of Ang Ⅱ or EGF (all 10-8 mol / L) 60%, and 102% respectively; (2) MAPK activity (γ32P incorporation) increased by 202% and 305%, respectively, after treatment with Ang Ⅱ (5 min) or EGF (3) liposome transfection method introduced antisense MAPK oligodeoxynucleotide (ODN) into FB, MAPK protein expression was significantly inhibited; Ang Ⅱ or EGF-induced FBDNA synthesis rate ratio Liposome control group decreased by 58% and 46%, the number of cells decreased by 38% and 44%; phosphorylated MAPK decreased by 85% and 90%, MAPK activity decreased by 74-2% and 5-9%. The results suggest that in the Ang Ⅱ or EGF-induced myocardial FB split reaction are MAP?