目的 探究碘缺乏大鼠肝脏、肾脏及海马组织中甲状腺激素[三碘甲状腺原氨酸（triiodothyronine,T3）、甲状腺素（thyroxine,T4）、反T3（reverse triiodothyronine,rT3）]的动态变化及其意义。方法 将36只SD大鼠按3个干预时间点（4、8、16 w）随机分配,每个时间点下设2个干预组（每组n=6）,分别为适碘（NI）组、碘缺乏（ID）组,各组均饲以碘缺乏饲料（碘含量50 μg/kg）,通过控制饮用水中的碘化钾（KI）浓度实现碘干预;干预结束时,使用冻存管收集大鼠肝脏、肾脏和海马组织,腹主动脉取血并分离血清,化学发光法评估甲状腺功能,ELISA法测定大鼠肝脏、肾脏和海马组织中甲状腺激素水平,Western blot检测肝脏、肾脏和海马组织中脱碘酶（deiodinase, Dio）的表达。结果 与NI组相比,ID组血清促甲状腺激素（thyroid stimulating hormone,TSH）水平在中后期代偿性升高（P<0.01）; 游离甲状腺素（free thyroxine,FT4）水平从第4 w起持续降低（P<0.05）;游离三碘甲状腺原氨酸（free triiodothyronine,FT3）水平在第8 w显著升高（P<0.01）,第16 w显著降低（P<0.01）。与NI组比较,ID组大鼠肝组织T3水平在早期显著降低,T4在后期降低;Dio1表达从第8 w开始显著高于对照组,而Dio3表达在早中期持续受到抑制,差异均有统计学意义（P<0.01）。与NI组比较,ID组大鼠肾组织T3、T4、rT3水平在第16 w均显著降低（P<0.01）;Dio1表达从第8 w开始高于对照组,Dio3表达则从第8 w起持续抑制,差异均有统计学意义（P<0.01）。与NI组比较,ID组大鼠海马组织中T3、T4水平在不同时点显著降低（P<0.05）;Dio2表达由早期降低转为第8 w升高,Dio3表达则由早期升高转为中后期持续抑制,差异均有统计学意义（P<0.01）。结论 长期碘缺乏下,大鼠肝脏与肾脏主要通过调控Dio1与Dio3表达,促进外周组织活性T3的生成与利用,适应全身代谢需求;与之不同,海马则通过对Dio2与Dio3的双向调节,维持脑内T3浓度的稳定,从而保护正常的神经功能。

Objective To investigate the dynamic changes and significance of thyroid hormones [triiodothyronine (T3), thyroxine (T4), reverse triiodothyronine (rT3)] in the liver, kidney, and hippocampus of iodine-deficient rats. Methods Thirty-six SD rats were randomly assigned to three intervention time points (4, 8, and 16 weeks). At each time point, two groups (n=6 per group) were established: the adequate iodine (NI) group and the iodine-deficient (ID) group. All rats were fed an iodine-deficient diet (iodine content <50 μg/kg), and iodine intervention was achieved by adjusting the concentration of potassium iodide (KI) in the drinking water. At the end of the intervention, rat liver, kidney, and hippocampal tissues were collected using cryovials. Serum was collected from abdominal aorta blood. Thyroid function was assessed by chemiluminescence immunoassay. Thyroid hormone levels in the liver, kidney, and hippocampus tissues were measured by ELISA, the expression of deiodinase (Dio) expression was analyzed by Western blot. Results Compared with the NI group, the ID group exhibited a compensatory increase in serum thyroid stimulating hormone (TSH) during the middle and late stages (P<0.01), along with a persistent decrease in free thyroxine (FT4) after week 4 feeding (P<0.05). Free triiodothyronine (FT3) levels showed a significant increase at week 8 (P<0.01) followed by a significant decrease at week 16 (P<0.01). Compared with the NI group, the ID group exhibited significantly decreased T3 levels in the liver during the early stage and decreased T4 levels during the late stage. Hepatic Dio1 expression was significantly upregulated after week 8 feeding, while Dio3 expression was continuously inhibited during the early and middle stages (all P < 0.01). In the kidney, T3, T4, and rT3 levels were significantly reduced at week 16 in the ID group (P<0.01). Renal Dio1 expression was elevated at week 8, whereas Dio3 expression was persistently inhibited after week 8 feeding (all P < 0.01). In the hippocampus, T3 and T4 levels were significantly decreased at multiple time points in the ID group (P<0.05). Hippocampal Dio2 expression initially decreased in the early stage and then increased by week 8, while Dio3 expression increased from the early stage to the late stage (all P<0.01). Conclusion Under chronic iodine deficiency, the liver and kidney response by modulating Dio1 and Dio3 expression to promote peripheral T3 secretion for systemic metabolic needs. Conversely, the hippocampus maintains cerebral T3 stability via bidirectional regulation of Dio2 and Dio3 expression, thereby preserving normal neural function.