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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±13.732),(26.342±7.303)pmol/(min.mg)略低于对照组(36.776±15.711)pmol/(min.mg),而胞膜PKC活性(33.221±18.341),(30.178±10.443)pmol/(min.mg)稍高于对照组(20.560±6.312)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±0.432,1.414±0.394)较对照组(0.649±0.294)升高,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 investigate the effects of iodine deficiency and hypothyroidism on protein kinase C (PKC) activity in hippocampus of offspring. Methods Low iodine diet and methimazole were used to establish animal model of hypothyroidism and hypothyroidism respectively. At the 30th day after birth, the rats in hypothyroid group, hypothyroidism group and control group were collected and the hippocampus Cytoplasm, cell membrane PKC activity. Results PKC activity (24.876 ± 13.732), (26.342 ± 7.303) pmol / (min.mg) in hippocampus of hypoxemia group and hypothyroidism group was slightly lower than that of control group (36.776 ± 15.711 pmol / (min.mg), while the membrane PKC activity (33.221 ± 18.341), (30.178 ± 10.443) pmol / (min.mg) was slightly higher than the control group (20.560 ± 6.312) pmol / (min.mg) (1.187 ± 0.432,1.414 ± 0.394) in hippocampus of hypothyroidism group were significantly higher than those in control group (0.649 ± 0.294), the difference was statistically significant (P <0.01). Conclusions Low iodine and hypothyroidism can cause the transport of PKC to the plasma membrane in the hippocampus of the offspring, which may be one of the mechanisms of hypokalemia and hypothyroidism that cause the impairment of learning and memory in the hippocampus.