摘要
目的 :研究丝裂原活化蛋白激酶 (MAPK )信号途径在缓激肽 (BK)介导的大鼠血管平滑肌细胞 (VSMC)增殖中的作用。方法 :通过 3H -胸苷 (3H- Td R)掺入率与 SMC3H-亮氨酸掺入率分别反映 VSMC的 DNA代谢与蛋白质合成代谢速率 ;并通过给予 PD0 980 5 9及 N-乙酰半胱氨酸预处理 ,观察其对细胞增殖的影响。结果 :1BK(10 nm ol/L )处理 30 min,VSMC3H-胸苷掺入率和 3H-亮氨酸掺入率均明显增高 ;2 BK增高 3H -胸苷掺入的作用可明显被PD0 980 5 9所抑制 ,对 3H -亮氨酸掺入的作用可部分被 PD0 980 5 9所抑制 ;3BK增高 3H -胸苷掺入和 3H -亮氨酸掺入的作用均可部分被 N-乙酰所抑制 ,完全被 N-乙酰 +PD0 980 5 9所抑制。结论 :细胞外信号调节激酶 (ERKs)激活在缓激肽介导的 VSMC增殖中具有重要作用 ,并可通过 ERKs信号途径的特异性抑制剂影响血管平滑肌细胞的增殖效应。
AIM: To investigate the role of mitogen-activated protein kinase signaling pathway in bradykinin-induced rat VSMC. METHODS:DNA synthesis ratio and protein synthesis ratio were quantified by thymidine incorporation, and by leucine incorporation respectively. Regulations of ERKs in bradykinin-induced proliferation were investigated by preincubation with either PD098059 or N-acetyl-L-cysteine. RESULTS:Our results indicated that Bradykinin(10 nmol/L) significantly increased thymidine incorporation and leucine incorporation.Preincubation of VSMC with PD098059 significantly inhibited the increase of thymidine incorporation and partly inhibited the increase of leucine incorporation induced by BK. Preincubation of VSMC with N-acetyl-L-cysteine partly inhibited the increase of thymidine incorporation and the increase of leucine incorporation induced by BK. Preincubation of VSMC with PD098059 +N-acetyl-L-cysteine completely inhibited the increase ofthymidine and leucine incorporations induced by BK. CONCLUSION:The activation of extracellular signal -regulated mitogen -activated protein kinase plays an important role in vascular smooth muscle cell growth and proliferation induced by bradykinin.
出处
《心脏杂志》
CAS
2004年第4期318-320,共3页
Chinese Heart Journal
