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目的 探讨钙调神经磷酸酶 (CaN)依赖的信号通路在三磷酸肌醇 (IP3)剌激的乳鼠心肌成纤维细胞 (FBs)增殖中的作用。方法 以培养的FBs为模型 ,用IP3剌激FBs内Ca2 +释放 ,环孢素A(CsA)阻断CaN ,维拉帕米 (Ver)阻断FBs钙通道 ,检测FBs的CaN、丝裂素活化蛋白激酶 (MAPK)、蛋白激酶C(PKC)活性 ,用3H 亮氨酸及3H 胸腺嘧啶掺入量作为反应FBs增殖的指标。结果 IP3剌激组FBs蛋白核酸合成速率明显增高 ,与对照组相比差异显著 (P <0 .0 1 ) ;CsA及Ver能明显抑制IP3介导的FBs蛋白核酸合成速率增高 ,与IP3剌激组相比差异显著 (P <0 .0 1 )。同时发现IP3剌激组CaN、PKC活性与对照FBs相比差异显著 (P <0 .0 5,P <0 .0 1 )。CsA和Ver抑制IP3介导的FBs的CaN活性增高 ,Ver抑制IP3介导的FBs的PKC活性增高。结论 CaN在IP3剌激的FBs增殖中起重要作用 ,但CaN信号通路不是IP3剌激FBs增殖的唯一信号通路 ,其它信号通路也可能参与了IP3剌激的FBs增殖。
Objective To investigate the role of calcineurin (CaN) -dependent signaling pathway in the proliferation of neonatal rat cardiac fibroblasts (FBs) stimulated with inositol 1,4,5-trisphosphate (IP3). Methods Using cultured FBs as a model, Ca2 + release from FBs was stimulated by IP3, CaN was blocked by CsA, and calcium channels were blocked by verapamil. The CaN, Activation of protein kinase (MAPK), protein kinase C (PKC) activity, with 3H-leucine and 3H thymidine incorporation as indicators of FBs proliferation reaction. Results The rate of nucleic acid synthesis of FBs protein in IP3 stimulation group was significantly higher than that in control group (P <0.01). CsA and Ver significantly inhibited the IP3-mediated increase of FBs protein synthesis rate, The difference was significant (P <0. 01). At the same time, it was found that the activity of CaN and PKC in IP3 stimulation group was significantly different from that in control FBs (P <0.05, P <0.01). CsA and Ver inhibited the IP3-mediated increase of CaN activity in FBs and Ver inhibited IP3-mediated increase of PKC activity in FBs. Conclusion CaN plays an important role in the proliferation of FBs stimulated by IP3. However, CaN signaling pathway is not the only signal pathway that IP3 stimulates the proliferation of FBs. Other signaling pathways may be involved in the proliferation of FBs stimulated by IP3.