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作 者:朱小虎[1] 王俊华[1] 李海峰[1] 王刚[1] 徐远红[1] 陈霞平[2]
机构地区:[1]湖北郧阳医学院附属太和医院康复医学科,十堰442000 [2]湖北郧阳医学院附属太和医院药学部,十堰442000
出 处:《中国新药杂志》2008年第1期40-42,46,共4页Chinese Journal of New Drugs
摘 要:目的:探讨双嘧达莫促进体外培养神经干细胞增殖的机制。方法:取新生小鼠大脑进行神经干细胞原代培养,以2.5μmol·L^(-1)双嘧达莫组作为阳性对照组,分别加入腺苷受体拮抗剂CGS15943和Trk受体拮抗剂K252a,通过观察神经球形态、神经球生成数目、MTT法定量,初步探讨双嘧达莫促神经干细胞增殖的机制。结果:K252a+双嘧达莫组神经球数量和细胞活性均明显低于双嘧达莫组(P<0,01),而CGS15943+双嘧达莫组与双嘧达莫组相比差异无统计学意义。结论:双嘧达莫的促神经干细胞增殖作用可能是通过Trk受体介导的。Objective:To study the mechanism of dipyridamole on proliferation of neural stem cells in vitro.Methods:Primary neural stem cells from newborn mice were treated with dipyridamole(2.5μmol·L^-1)a- lone or combination with K252a,an antagonist of Trk receptor,and CGS15943,one of the antagonists of non-selec- tive adenosine receptor.The shape and number of the newly generated neurospheres were observed under a convert phase microscope.The neurosphere numbers were counted,and its viability was determined by MTT reduction assay.Results:The number and viability of the neurospheres were significantly decreased after treatment with K252a+dipyridamole as compared with dipyridamole alone.Conclusion:The promoting effect of dipyridamole on proliferation of neural stem cells may be mediated by Trk receptor activation.
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