中文摘要：

目的观察副交感神经递质乙酰胆碱及其特异性浕7 n型乙酰胆碱受体拮抗剂甲基牛扁碱对培养的小鼠前脂肪细胞的作用,对其机制进行探讨。方法乙酰胆碱刺激细胞后采用MTT观察细胞增殖能力,ELISA检测上清中白细胞介素6和10的动态变化,免疫印迹法检测核因子κB p65蛋白水平。结果乙酰胆碱促进前脂肪细胞增殖,12 h为对照组的122.0%±11.4%,甲基牛扁碱能够阻断其对细胞增殖的作用;乙酰胆碱刺激细胞分泌白细胞介素6,6 h后达到高峰,同时抑制细胞分泌白细胞介素10,12 h后明显降低,持续至24 h,甲基牛扁碱对细胞因子的分泌无明显作用;乙酰胆碱上调核因子κB p65蛋白水平,6 h达顶峰,此后逐渐下降,但24 h时仍明显高于对照水平,甲基牛扁碱不能够阻断该效应。结论副交感神经递质乙酰胆碱可能通过促进前脂肪细胞核因子κB p65蛋白核转位激活前脂肪细胞,促进炎症反应,甲基牛扁碱对此无明显作用,提示细胞表面浕7 n型乙酰胆碱受体并非其作用的主要受体。

英文摘要：

Aim To assess the effect of acetylcholine（Ach） and its antagonist methyllycaconitine（MLA） on murine preadipocytes. Methods MTT was used for the proliferation ability examination.ELISA was used for IL-6 and IL-10.Western blotting was used for NF-κB p65 protein in nucleus. Results Ach could promote preadipocytes proliferation,with 122.0%±11.4% compared to control after stimulation for 12 h,and MLA could block its effect.Ach could induce preadipocytes secret IL-6 and reach its peak at 6 h,significantly higher than that of control group（P0.05）.Ach could decrease IL-10 concentration.MLA had little effect on cytokines secretion.Ach could increase the level of NF-κB p65 in nucleus,with the highest level at 6 h.MLA couldn＇t block its effect. Conclusion Ach could activate preadipocytes through promoting NF-κB p65 protein translocation.MLA couldn＇t antagonize its action,suggesting that ɑ7 n Ach receptor,which is the major receptor through which Ach exerts its anti-inflammation effect,didn＇t play an important role in the process.