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作 者:王晓东[1]
出 处:《中华内分泌代谢杂志》1993年第1期38-39,共2页Chinese Journal of Endocrinology and Metabolism
摘 要:作者使用Fura-2作为Ca^(++)指示剂,观察了促甲状腺激素释放激素(TRH)和白细胞介素-1β(IL—1β)对体外培养的大鼠GH_3垂体细胞内Ca^(++)([Ca^(++)]i)水平的影响。结果显示10^(-7)~10^(-9)mol/L浓度TRH促进[Ca^(++)]i动员,其程度呈TRH剂量依赖性。单用0.01~10U/ml IL—1β未增加工[Ca^(++)]i水平。用0.1U/ml IL—1β与待测细胞温育1和3分钟后,加入TRH,[Ca^(++)]i释放则受明显抑制;而TRH与IL—1β同时使用,抑制作用则明显减弱。本研究证实[Ca^(++)]i对TRH在垂体细胞内的作用起重要信息传递作用,一定剂量IL—1β可能通过抑制TRH诱导的[Ca^(++)]i释放影响垂体功能。The effects of TRH and recombinant human IL-1β on cytosolic free calcium mobilization in rat GH, pituitary cells cultured in vitro was studied spectrofluorometrically using Fura-2 as Ga++ indicator. The results showed that TRH 10-7~10-9mol/L stimulated the cytosolic Ca++mobilization in a dose-dependent manner. IL-1 alone in the concentration ranging from 0.01 to 10 U/ml did not increase the intracellular Ca++ level. 1- and 3-minute pretreatment of the GH3 cells with IL-1β 0.1 U/ml significantly inhibited TRH-induced Ca++ mobilization, whereas such suppressive effects were significantly diminished when IL-1/3 and TRH were added at the same time. These findings suggest that Ca++ may signal a TRH effect in pituitary cells and IL-1β influences pituitary function by inhibiting Ca++ mobilization induced by TRH.
分 类 号:R335.1[医药卫生—人体生理学]
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