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作 者:夏春芳[1] 霍勇[1] 尹航[1] 朱国英[1] 庞永正[1] 唐朝枢[1]
出 处:《中国动脉硬化杂志》2001年第3期213-216,共4页Chinese Journal of Arteriosclerosis
摘 要:为探讨白细胞介素 10抑制血管紧张素Ⅱ诱导的大鼠血管平滑肌细胞增殖的细胞信号机制 ,采用3 H -TdR掺入的方法检测血管平滑肌细胞DNA合成 ,3 2 P ATP掺入检测丝裂素活化蛋白激酶和蛋白激酶C活性 ,蛋白免疫印迹杂交及免疫沉淀方法检测粘着斑激酶蛋白表达及其活性变化。结果显示 ,白细胞介素 10呈浓度依赖性抑制血管紧张素Ⅱ诱导的血管平滑肌细胞增殖 ,同时下调血管紧张素Ⅱ引起的丝裂素活化蛋白激酶、蛋白激酶C和粘着斑激酶信号的激活 (P <0 .0 5或P <0 .0 1)。因此白细胞介素 10可能通过下调血管紧张素Ⅱ刺激的丝裂素活化蛋白激酶。Aim To investigate the possible signal transduction pathway by which IL 10 inhibits the proliferation of vascular smooth muscle cells (VSMC) induced by angiotensin Ⅱ (AngⅡ). Methods 3 H TdR and 32 P ATP incorporation were used to detect the proliferation of VSMC and the activity of mitogen activity proteinkinase(MAPK) and protein kinase C (PKC), respectively. Western blot and immunoprecipitation were applied to assay the expression and activity of focal adhesion kinase (FAK), respectively. Results IL 10 inhibited VSMC proliferation induced by AngⅡ, and down regulated AngⅡ induced activition of MAPK, PKC and FAK(P<0.05 or P<0.01). Conclusions The results suggest that the inhibiting effect of IL 10 on AngⅡ stimulated VSMC proliferation may be mediated by down regulating MAPK, PKC and FAK activity stimulated by AngⅡ.
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