论文部分内容阅读
给小鼠用丙基硫氧嘧啶(PTU)抑制其体内甲状腺激素的合成以制备实验性“甲低”小鼠模型。该鼠脾淋巴细胞的增殖反应及白细胞介素II(IL-2)的生成均明显低于对照小鼠,给“甲低”小鼠补充不同剂量的L-T_4后,其脾淋巴细胞增殖反应随血中T_3、T_4水平的恢复呈剂量依赖性增强,当剂量过大(10mg/kg)时,血中T_3、T_4含量明显高于正常,此时,脾淋巴细胞增殖反应反而下降。将正常小鼠的脾淋巴细胞在体外培养,加入L-T_2(10~(14)～10~(-6)或L-T_4(10~(-12)～10~(-4)均可剂量依赖性地促进ConA诱导的脾淋巴细胞增殖,分别在10~(-10)M及10~(-2)M时达最大效应,剂量进一步增加,增殖反应反而下降,这与体内实验结果基本一致。在加了L-T_4且经48小时培养的脾淋巴细胞上清液中未检出T_3,表明L-_4不需转变为T_3即可发挥作用,即T_3、T_4均能直接影响脾淋巴细胞的增殖。本实验结果证明甲状腺激素在体内外均能促进T淋巴细胞增殖,其机制与促进IL-2生成有关。
Mice were challenged with propylthiouracil (PTU) to inhibit their thyroid hormone synthesis in vivo to prepare experimental “hypoglycemic” mouse models. The proliferative response of splenic lymphocytes and the production of interleukin-2 (IL-2) were significantly lower than those of the control mice. After the L-T 4 mice were given different doses of L-T 4, their spleen lymphocyte proliferation reaction With the recovery of T_3 and T_4 levels in blood, the dose-dependent increase of T_3 and T_4 levels was observed. When the dose was too high (10 mg / kg), the content of T_3 and T_4 in blood was significantly higher than normal. The splenic lymphocytes of normal mice were cultured in vitro and the dose of L-T 2 (10 ~ (14) ~ 10 ~ (-6)) or L-T_4 (10 ~ (-12) ~ 10 ~ (-4) Dependently promoted the proliferation of ConA-induced splenic lymphocytes, which reached the maximum effect at 10 ~ (-10) M and 10 ~ (-2) M, respectively. The dose was further increased and the proliferative response decreased, which was consistent with the in vivo experimental results T_3 was not detected in the supernatant of L-T_4-splenic lymphocytes cultured for 48 hours, indicating that L__4 did not need to be changed to T_3, that is, T_3 and T_4 could directly affect spleen lymphocytes Of the proliferation of the experimental results show that thyroid hormone can promote T lymphocyte proliferation both in vitro and in vivo, and its mechanism and promote IL-2 production.