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目的:探讨醛固酮诱导心肌成纤维细胞(CFs)增殖的信号转导机制。方法:用胰酶消化法分离、培养新生大鼠CFs,采用3H-胸腺嘧啶核苷(3H-TdR)掺入法、western-blotting技术从DNA合成、蛋白表达等方面观察MAPK活化与醛固酮促CFs增殖的关系。结果:①醛固酮剂量依赖性促CFsDNA合成,10-5mol/LPD98059[(782±152)个·min-1]可逆转10-7mol/L醛固酮[(1879±169)个·min-1]的作用;②10-7mol/L醛固酮对活化MAPK蛋白表达有显著增强作用,在4h达峰作用(8.11±0.46),10-7mol/L醛固酮的作用(8.11±0.46)被10-5mol/LPD98059(1.21±0.10,P<0.01)阻断。结论:醛固酮能激活CFs的MAPK,MAPK表达及活化参与醛固酮诱导的CFs增殖。
Objective: To investigate the signal transduction mechanism of aldosterone-induced proliferation of cardiac fibroblasts (CFs). Methods: Newborn rat CFs were isolated and cultured by trypsin digestion. 3H-thymidine (3H-TdR) incorporation and western-blotting were used to observe the effects of MAPK activation and aldosterone-induced CFs Proliferation relationship. Results: ① Aldosterone dose-dependently stimulated the synthesis of CFs by 10-5mol / L PD98059 [(782 ± 152) min-1], reversing the effect of 10-7mol / L aldosterone [(1879 ± 169) min-1] (8.11 ± 0.46), and the effect of 10-7mol / L aldosterone (8.11 ± 0.46) was significantly enhanced by 10-5mol / LPD98059 (1.21 ± 0.10, P <0.01). CONCLUSION: Aldosterone can activate MAPK and MAPK expression in CFs and their activation is involved in aldosterone-induced CFs proliferation.