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目的:观察亮氨酸脑啡肽(L-Enk)和脂多糖(LPS)对血管平滑肌细胞(VSMC)增殖的影响,并观察两者之间的相互作用及阿片受体阻滞剂纳络酮(Nal)的影响.方法:实验以离体培养的SD大鼠胸主动脉VSMC为模型.用四唑盐比色实验(MTT)法及3H-TdR掺入技术观察VSMC的增殖、DNA合成量的变化.结果:研究发现10-7kg/L~10-5kg/LLPS可显著促进VSMC的增殖及DNA的合成(P<0.05).10-5mol/L~10-4mol/LL-Enk对VSMC的增殖及DNA的合成有抑制作用(P<0.01).10-8mol/L~10-5mol/LNal对VSMC的增殖及DNA的合成无显著影响.L-Enk可抑制LPS促VSMC增殖的作用,此抑制作用可被Nal阻断.结论:LPS促进VSMC的增殖和DNA合成,L-Enk可抑制LPS的促VSMC增殖作用,该抑制作用是通过阿片受体介导的.
OBJECTIVE: To observe the effects of L-Enk and LPS on the proliferation of vascular smooth muscle cells (VSMCs) and to observe the interaction between the two and the opioid receptor blocker naloxone (Nal) influence. Methods: In vitro cultured rat aorta VSMC model of SD rats. The proliferation and the amount of DNA synthesis of VSMC were observed by MTT assay and 3H-TdR incorporation assay. Results: It was found that 10-7kg / L ~ 10-5kg / LLPS can significantly promote VSMC proliferation and DNA synthesis (P <0.05). 10-5mol / L ~ 10-4mol / LL-Enk inhibited VSMC proliferation and DNA synthesis (P <0.01). 10-8mol / L ~ 10-5mol / LNal VSMC proliferation and DNA synthesis had no significant effect. L-Enk can inhibit the proliferation of LPS-induced VSMC, this inhibition can be blocked by Nal. Conclusion: LPS can promote VSMC proliferation and DNA synthesis. L-Enk can inhibit LPS-induced VSMC proliferation, which is mediated by opioid receptors.