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作 者:殷洪博[1] 刘长晟[1] 王萍[1] 陈新秋[1] 刘万洋[2] 董静[2] 陈杰[2] 吴泽明[3]
机构地区:[1]沈阳市疾病预防控制中心,110031 [2]中国医科大学公共卫生学院 [3]沈阳市卫生局
出 处:《中国公共卫生》2005年第10期1170-1171,共2页Chinese Journal of Public Health
摘 要:目的研究碘缺乏、甲状腺功能减退对仔鼠海马蛋白激酶C(PKC)活性的影响。方法分别选用低碘饲料及他巴唑诱导建立低碘及甲减大鼠动物模型,在生后第30 d时收集低碘组、甲状腺功能减退组及对照组大鼠仔鼠海马组织,测定海马细胞浆、细胞膜PKC活性。结果生后30 d低碘组和甲状腺功能减退组仔鼠海马胞液PKC活性(24.876 3±13.731 9),(26.342 0±7.302 8)pmol/(min.mg)略低于对照组(36.775 8±15.711 3)pmol/(min.mg);而胞膜PKC活性(33.220 7±18.341 4),(30.177 5±10.443 3)稍高于对照组(20.559 8±6.312 1)pmol/(min.mg),低碘组、甲状腺功能减退组仔鼠海马胞膜PKC活性与胞浆PKC活性比值(1.187 1±0.432 5),(1.414 3±0.394 0)较对照组升高(0.649 3±0.294 3),差异有统计学意义(P<0.01)。结论低碘、甲状腺功能减退可引起仔鼠海马胞浆PKC向胞膜的转运,可能是低碘、甲减引起海马损害导致学习记忆功能减退的机制之一。Objective To study the effects of iodine deficiency and hypothyroidism on activity of protein kinase C(PKC) in rat pups hippocampus, Methods Iodine deficient rats were administered with iodine-deficient diet and hypothyroid rats were administered with methimazole in drinking water, On postnatal 30 days, the hippocampus from the three groups was separated from the brain for PKC activity detection. Results Cytosol PKC activities in iodine deficient and hypothyroid groups(24. 876 3 ± 10. 443 3 ) were higher than that of the control group (20. 559 8 ± 6.312 1 ) pmol/( min· mg). PKC activities(membrane/cytosol) in iodine deficient ( 1.187 1 ± 0. 432 5 ) and hypothyroid( 1.414 3 ± 0. 394 0 ) groups were significantly higher than that of the control group (0. 649 3 ± 0. 294 3 ) ( P 〈 0.01 ). Conclusion Iodine deficiency and hypothyroidism during critical periods brain developent may promote translocation of PKC from the cytosol to the membrane fraction and contribute to cognitive deficits associated with developmental iodine deficiency and hypothyroidism.
关 键 词:碘缺乏:甲状腺功能减退 大鼠海马 蛋白激酶C
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