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作 者:张曜文[1] 阳乔[1] 刘红艳[1] 唐望先[1]
机构地区:[1]华中科技大学同济医学院附属同济医院肝病研究所,湖北武汉430030
出 处:《胃肠病学和肝病学杂志》2009年第3期228-230,共3页Chinese Journal of Gastroenterology and Hepatology
基 金:国家自然科学基金资助项目(30571627)
摘 要:目的探讨内源性大麻素(anandamide,AEA)对肝组织神经末梢去甲肾上腺素(NE)的影响及可能的神经生物学机制。方法制备小鼠肝突触小体,用高效液相色谱-电化学(HPLC-ECD)方法检测AEA在体外对肝突触小体NE递质的影响。结果小鼠肝突触小体分离成功,体外实验中随着AEA浓度逐渐升高至10μmol/L,肝突触小体内NE的含量减少27.81%~70.79%,存在明显的剂量效应关系,差异有统计学意义(P〈0.01);AEA浓度继续升高时,去甲肾上腺素含量不再继续减少。结论AEA能通过干扰小鼠肝突触部位NE递质的再摄取,产生抑制性作用。Objective To study the effect of anandamide (AEA) on the uptake of repinephrine (NE) in nerve terminal of liver and to investigate its possible neurobiological mechanism. Methods The mice liver synaptosomes were prepared in vitro. The contents of norepinephrine in liver synaptosomes were detected by high performance liquid chromatography-electrochemical detector (HPLC-ECD). Results Mice liver synaptosomes was separated successfully. With the increase of exposure to AEA (1 -10 μmol/L) , the uptake of repinephrine was decreased by 27.81% -70.79%. There was a dose-effect relation between them and the difference of the results was significant. Then, the uptake of repinephrine would not continue to decrease if the density of AEA exceeded 10 μmol/L. Conclusion AEA can interfere with the uptake of repinephrine transmitter in mice liver synaptosomes and cause inhibitive effects.
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