Dose-response and time course of hypothyroxinemia and hypoinsulinemia and characterization of insulin hypersensitivity in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated rats

Male Sprague-Dawley rats were administered i.p. various doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in corn oil. At several time points thyroid stimulating hormone (TSH), total thyroxine (TT4), free thyroxine (FT4), total triiodothyronine (TT3), reverse triiodothyronine (rT3) and insulin were determined in serum using radioimmunoassays, and glucose was measured by the glucose oxidase method. TSH and TT3 were not affected by any dose at any time point of measurement. TT4 and FT4 were decreased in a somewhat dose-dependent manner by days 2 to 4 after dosing. Return of TT4 and FT4 to normal values by day 32 after TCDD dosage also occurred in a dose-dependent manner, except in rats that died later. rT3 was also decreased at each dose level early and returned to normal levels in a somewhat dose-dependent fashion. Rats in the 2 highest dose groups became hypoinsulinemic and in the highest dose group also hypoglycemic by day 8 after dosing. Serum insulin and glucose remained suppressed in non-survivors of TCDD until death ensued. In survivors, serum insulin returned to normal values by day 32 after dosing. The hypoinsulinemic state was further characterized by hypersensitivity towards insulin, i.e. injection of an otherwise non-toxic dose of insulin 3 days after administration of 125 micrograms/kg TCDD was lethal to 80% of the rats within 24 h. Insulin hypersensitivity preceded both hypoglycemia and hypoinsulinemia. These findings suggest that hypothyroxinemia and hypoinsulinemia may be part of an adaptive process whereby rats attempt to diminish the toxic insult of TCDD.     

Dietary high-fat lard intake induces thyroid dysfunction and abnormal morphology in rats

Aim:

Excess dietary fat intake can induce lipotoxicity in non-adipose tissues. The aim of this study was to observe the effects of dietary high-fat lard intake on thyroid in rats.

Methods:

Male Sprague-Dawley rats were fed a high-fat lard diet for 24 weeks, and then the rats were fed a normal control diet (acute dietary modification) or the high-fat lard diet for another 6 weeks. The serum lipid profile, total thyroxine (TT4), free thyroxine (FT4) and thyrotropin (TSH) levels were determined at the 12, 18, 24 and 30 weeks. High-frequency ultrasound scanning of the thyroid glands was performed at the 24 or 30 weeks. After the rats were sacrificed, the thyroid glands were collected for histological and immunohistochemical analyses.

Results:

The high-fat lard diet significantly increased triglyceride levels in both the serum and thyroid, and decreased serum TT4 and FT4 levels in parallel with elevated serum TSH levels. Ultrasonic imaging revealed enlarged thyroid glands with lowered echotexture and relatively heterogeneous features in the high-fat lard fed rats. The thyroid glands from the high-fat lard fed rats exhibited enlarged follicle cavities and flattened follicular epithelial cells under light microscopy, and dilated endoplasmic reticulum cisternae, twisted nuclei, fewer microvilli and secretory vesicles under transmission electron microscopy. Furthermore, the thyroid glands from the high-fat lard fed rats showed markedly low levels of thyroid hormone synthesis-related proteins TTF-1 and NIS. Acute dietary modification by withdrawal of the high-fat lard diet for 6 weeks failed to ameliorate the high-fat lard diet-induced thyroid changes.

Conclusion:

Dietary high-fat lard intake induces significant thyroid dysfunction and abnormal morphology in rats, which can not be corrected by short-term dietary modification.     

皮质醇增多症治疗控制对促甲状腺素和甲状腺激素水平的影响

观察10例皮质醇增多症未治患者和8例治疗控制患者血中促甲状腺素（TSH）和甲状腺激素浓度的改变。结果显示未治组平均TSH、TT3、FT3血浓度明显低于正常低限，TT4稍低于正常，FT4略高于正常低限。治疗控制组平均TSH、TT3、FT3浓度明显上升，与未治组比较差别有显著性意义；TT4、FT4稍上升，与未治组比较差别无挺着性意义。在治疗技制组除TT3略低于正常外，TSH、FT3、TT4平均值均恢复正常。提示皮质醇增多症治疗控制后，合并存在的下丘脑－垂体－甲状腺轮功能紊乱可随之恢复。     

猫爪草粗多糖治疗自身免疫性甲状腺炎的实验研究

目的 研究猫爪草粗多糖对实验性自身免疫性甲状腺炎（EAT）小鼠免疫干预作用。方法 雌性BALB/C小鼠多点皮下注射甲状腺球蛋白辅以佐剂,配合饮用高碘水,形成实验性自身免疫性甲状腺炎模型,用药干预。用化学发光法检测实验性自身免疫性甲状腺炎小鼠血清甲状腺素（TT4）、三碘甲状腺原氨酸（TT3）、游离甲状腺素（FT4）、游离三碘甲状腺原氨酸（FT3）、高灵敏人促甲状腺激素（TSH）;用放射免疫法检测抗甲状腺球蛋白抗体（TGAb）、抗甲状腺微粒体抗体（TMAb）。结果 与正常组相比,实验性自身免疫性甲状腺炎小鼠血清甲状腺素、游离甲状腺素、游离三碘甲状腺原氨酸显著降低（P<0.01）,高灵敏人促甲状腺激素、抗甲状腺球蛋白抗体、抗甲状腺微粒体抗体显著升高（P<0.01）;三碘甲状腺原氨酸与正常组无显著性差异。用药治疗后,与模型组相比,猫爪草粗多糖各剂量组甲状腺素、游离甲状腺素、游离三碘甲状腺原氨酸水平显著回升（P<0.01）,抗甲状腺球蛋白抗体、抗甲状腺微粒体抗体水平仍旧处于高位。结论 实验性自身免疫性甲状腺炎小鼠处于甲减状态,猫爪草粗多糖能在一定程度上干预实验性自身免疫性甲状腺炎小鼠的甲状腺激素水平,有利于其恢复,其作用可能与其抗炎及免疫调节功能有关。     

肝硬化病人下丘脑-垂体-甲状腺轴的功能变化及临床意义

目的 探讨不同级别肝硬化(LC)病人下丘脑-垂体-甲状腺轴的变化及临床意义.方法 91例LC病人按Child-Turcotte-Pugh(CTP)计分评级分为三组:LC-A组25例,LC-B组35例,LC-C组31例;另选27名健康人作为对照组.血清总三碘甲状腺原氨酸(TT3)、游离T3(FT3)、反T3(rT3)、总甲状腺素(TT4)、游离甲状腺素(FT4) 及促甲状腺激素(TSH) 均采用化学发光法检测,肝功能生化指标用RXL生化分析仪检测,凝血酶原时间(PT)用全自动血凝仪(血凝固法)检测.结果 从LC-A组到LC-C组随着肝硬化级别的增加,血清TT3和FT3水平逐渐降低,rT3渐次增高,TT4/rT3比值顺次下降,血清TT3分别与白蛋白、前白蛋白、载脂蛋白-A1和胆碱酯酶呈显著正相关(df=89,r值分别为0.568,0.260,0.317和0.599,P<0.05),与CTP分值及PT呈显著负相关(df=89,r值分别为-0.447和-0.297,P<0.01),TSH在各组间差异无统计学意义.共26例LC病人出现低T3综合征,LC-A组为0,LC-B组8例(22.9%),LC-C组18例(58.1%).经保肝、支持治疗1~2周后,随着肝功能好转低T3综合征也随之消失.心得安试验仅见FT4有所下降(16.84±3.16)vs (14.00±2.45) pmol·L-1,地塞米松试验未见甲状腺激素及TSH有明显变化.结论 肝硬化失代偿期随着肝功能的下降,发生低T3综合征的比例增多,与甲状腺激素转运蛋白合成功能减退、T4向T3转化减少有关,但随着病情好转低T3综合征便逐渐消失,无须补充甲状腺素.心得安或地塞米松试验对甲状腺功能未产生明显的影响,提示短期适量应用此类药物是安全的.     

早产儿暂时性甲状腺功能障碍分析与治疗

目的探讨早产儿暂时性甲状腺功能障碍的情况及左旋甲状腺素治疗的疗效。方法对165例早产儿进行血清FT4、T4、FT3、T3、TSH检测,对FT4、T4降低的早产儿按甲状腺功能低下症状有无分为观察组与对照组,对T3降低的早产儿随机分为观察组与对照组,观察组予左旋甲状腺素治疗,定期复查血清FT4、T4、FT3、T3、TSH。结果①早产儿暂时胜甲状腺功能障碍发生率为47．27％,胎龄越小,发生率越高。其中胎龄28～30周发生率为77．27％,30。32周75％,32—34周39．47％,34～36周32．47％。②低甲状腺素血症观察组早产儿经左旋甲状腺素治疗后症状消失,血清FT4及T4恢复正常时间较对照组快。生后14天观察组FT4、T3 100％恢复正常,对照组44．4％恢复正常,P=0．00。③低T3综合征早产儿观察组与对照组的TSH、T3恢复正常所需时间无差别。生后28天观察组TSH、T315％恢复正常,对照组10％恢复正常,P=1．00。结论早产儿生后甲状腺功能暂时性低下,胎龄越小,功能越低。对于有甲状腺功能低下临床症状的早产儿予短期左旋甲状腺素治疗有助于改善甲状腺功能。     

The effects of ranitidine on pituitary-thyroid function.

Although several studies have examined the effects of cimetidine on pituitary-thyroid function, few have investigated ranitidine in this respect. We found no changes in thyroid-stimulating-hormone (TSH) or prolactin responses to TSH-releasing-hormone (TRH) in 10 patients with peptic ulcer disease given oral ranitidine. Serum total and free thyroxine (TT4 and FT4) concentrations declined slightly, whereas total and free triiodothyronine (TT3 and FT3) increased slightly following ranitidine. None of these changes achieved statistical significance. Both the ratio of TT4/TT3 and FT4/FT3, however, declined (P less than 0.05) following ranitidine. Thus ranitidine may have a minor influence on peripheral deiodination of thyroxine but has little effect on hormone production from the thyroid gland. The diagnostic value of biochemical tests of thyroid function is not seriously compromised in patients receiving ranitidine.     

急性心力衰竭患者甲状腺激素改变的临床意义

目的观察急性心力衰竭(acute heart failure,AHF)患者甲状腺激素水平的变化情况。方法用放射免疫方法分析检测50例急性心力衰竭(AHF组)患者甲状腺激素水平和50例健康志愿者(对照组)血清甲状腺激素水平。结果AHF组与对照组相比,血清TT3、FT3值和TT4、FT4值下降,有显著性差异(P<0.05)。测TSH值,两组数值相近,比较无显著性差异(P>0.05)。结论急性心力衰竭患者血清T3、T4水平会下降。可借助血清T4、T3变化预测AHF患者的预后。     

Thyroid functions in pre-eclampsia and its correlation with maternal age, parity, severity of blood pressure and serum albumin.

Maternal thyroid function was investigated in 32 pre-eclamptic women and 10 normal pregnant women in their third trimester. Serum total tri-iodothyronine (TT3) and total thyroxine (TT4) were decreased significantly (P < 0.001) and TSH was increased significantly (P < .001) in pre-eclampsia as compared to normal pregnancy. There was no influence of parity and maternal age on thyroid functions. TT3 and TT4 decreased significantly (P < .001) with increase of serum albumin, while there was no correlation of TT4 with serum albumin.     

慢性心力衰竭患者甲状腺激素水平的变化

目的 探讨充血性心力衰竭（CHF）患者血清甲状腺激素水平的改变情况及其与病情的关系.方法 采用放射免疫法测定50例CHF患者（心功能Ⅱ级7例,Ⅲ级19例,Ⅳ级24例）和30例健康人血清三碘甲状腺原氨酸（T3）、四碘甲状腺原氨酸（T4）、游离三碘甲状腺原氨酸（FT3）、游离四碘甲状腺原氨酸（FT4）、促甲状腺激素（TSH）.结果 CHF组T3、FT3含量（1.95±0.55）nmol/L、（2.20±0.39）nmol/L,低于对照组的（2.4±0.50）nmol/L、（5.89±0.45）nmol/L（t=2.415,2.325,P〈0.05）;治疗后T3、FT3含量（2.19±0.53）nmol/L、（3.69±0.57）nmol/L,较治疗前显著升高（t=2.375,2.405,P〈0.05）;CHF心功能Ⅳ级患者T3、FT3含量（1.76±0.7）nmol/L、（1.99±0.45）nmol/L,明显低于对照组（t=2.245,2.375,P〈0.05）;血清TT3、TT4与心功能分级呈负相关（r=-0.933,-0.383,P均〈0.05）,血清FT3、FT4、TSH与心功能分级均无相关性.结论 血清甲状腺激素水平的改变可作为判断CHF严重程度的指标之一.     

老年2型糖尿病甲状腺激素水平与代谢指标相关性分析

目的分析老年2型糖尿病甲状腺激素水平与代谢指标的相关性。方法选择2010年1月至2012年6月于我院就诊的300例老年2型糖尿病患者作实验组,并按照糖化血红蛋白水平分为四组。选择健康体检者300例作正常对照组。分别检测所有试验者的甲状腺素总量（TT4）、游离甲状腺素（FT4）、游离甲腺原氨酸（FT3）、促甲状腺激素（TSH）和血清三碘甲腺原氨酸总量（TT3）,并对其进行比较。结果实验组患者的FT3、TT3均明显低于正常对照组,差异有统计学意义（P〈0．05）;GHbAIc〈6．5％组患者的Fr3、Tr3明显高于GHbAl（6．5％-7．5％）组、GHbAle（7．6％-10．0％）组、GHbAlc〉10．0％组,差异有统计学意义（P〈0．05）。各组患者的TT4、FT4、TSH比较,差异无统计学意义（P〉0．05）。结论准确检测患者的甲状腺激素代谢指标对老年2型糖尿病患者的病情控制有重要意义。     

JNK pathway decreases thyroid hormones via TRH receptor: A novel mechanism for disturbance of thyroid hormone homeostasis by PCB153

PCBs, widespread and well-characterized endocrine disruptors, cause the disruption of thyroid hormone (TH) homeostasis in humans and animals. In order to verify the hypotheses that MAPK pathways would play roles in disturbance of TH levels caused by PCBs, and that TH-associated receptors could function in certain MAPK pathway, Sprague-Dawley rats were dosed with PCB153 intraperitoneally (i.p.) at 0, 4, 16 and 32mg/kg for 5 consecutive days, and Nthy-ori 3-1 cells were treated with PCB153 (0, 1, 5, 10μM) for 30min. Results showed that after the treatment with PCB153, serum total thyroxine (TT4), free thyroxine (FT4), total triiodothyronine (TT3) and thyrotropin releasing hormone (TRH) were decreased, whereas free triiodothyronine (FT3) and serum thyroid stimulating hormone (TSH) were not altered. In vivo and in vitro studies indicated that JNK pathway was activated after PCB153 exposure. Moreover, TRH receptor (TRHr) level was suppressed after the activation of JNK pathway and was elevated after the inhibition of JNK pathway, but TSH receptor (TSHr) level was not affected by the status of JNK pathway though it was reduced after PCB153 treatment. The activated signs of ERK and P38 pathways were not observed in this study. Taken together, observed effects suggested that JNK pathway could decrease TH levels via TRHr, and that would be one novel mechanism of PCB153-mediated disruption of THs.     

小儿原发性肾病综合征的血清甲状腺激素水平临床分析

目的研究小儿原发性肾病综合征同血清甲状腺激素水平间的关系。方法选择本院64例原发性肾病综合征患儿,作观察组,同期入院体检的64例同龄健康儿童作对照组,检测两组儿童的血清甲状腺激素水平和蛋白水平,对比分析检测结果。结果观察组患儿的血清游离三碘甲腺原氨酸（FT3）和血清游离甲状腺素（FT4）水平均要明显低于对照组,促甲状腺激素（TSH）水平明显高于对照组,上述差异具有统计学意义（P〈0.05）;经直线相关分析,FT3和FT4同血清白蛋白水平呈正相关,同24h尿蛋白呈负相关,TSH同血清蛋白水平无显著相关性。结论 FT3、FT4同血清蛋白有着密切的联系,甲状腺激素水平的检测利于原发性肾病综合征的临床治疗。     

原发性高血压病人血清甲状腺激素水平的改变

目的 研究原发性高血压病人血清甲状腺激素水平的改变。方法 用放射免疫分析法测定38例高血压病人和20例健康对照者的血清甲状腺激素水平。结果 原发性高血压病人的血TT3、FT3值明显低于正常人,rT3值明显高于正常人,而TT4、FT4、TSH水平与正常组相比差异无显著意义;血TT3、FT3值的和rT3值的升高与高血压病的严重程度有关而与病程无关。结论 原发性高血压常伴有低血清TT3、FT3水平,且随着高血压病情的加重而逐渐降低。     

慢性充血性心力衰竭患者甲状腺素的变化

目的 研究甲状腺激素(thyroid hormone,TH)水平与慢性充血性心力衰竭(congestive heart failure,CHF)的关系.方法 应用微粒子发光法检测100例老年慢性充血性心力衰竭住院患者及50例健康对照者的血清三碘甲腺原氨酸(FT3)、总三碘甲腺原氨酸(TT3)、游离甲状腺素(FT4)、总甲状腺素(TT4)、反三碘甲腺原氨酸(rT3)及促甲状腺素(TSH)结果老年慢性充血性心力衰竭患者甲状腺素T3水平明显低于健康对照组,低T3综合征的老年CHF患者心力衰竭程度严重.结论 在早期慢性心力衰竭的患者,其T3水平是降低的,且与心力衰竭的严重程度有关.     

Increased biliary excretion of thyroxine by microsomal enzyme inducers.

The extrathyroidal mechanism by which endocrine disruptors promote thyroid tumors has been proposed to be increased glucuronidation and biliary elimination of thyroxine (T(4)), followed by disruption of the hypothalamic-pituitary-thyroid axis. The ability of a chemical to increase T(4) glucuronidation in vitro correlates with the ability to reduce serum T(4) concentrations. Pregnenolone-16alpha-carbonitrile (PCN), 3-methylchloranthrene (3-MC), and Aroclor 1254 (PCB) each increase T(4) glucuronidation in rat liver microsomes and reduce serum T(4). However, whether reductions in serum T(4) result directly from increases in T(4) glucuronidation and biliary excretion in vivo has not been thoroughly examined. It is also unclear whether reduced serum T(4) concentrations following microsomal enzyme inducer treatment elicit increases in serum thyrotropin (TSH), the primary stimulus for thyroid cell proliferation, because only PCN treatment increases serum TSH. This study sought to determine whether increases in T(4)-glucuronide biliary excretion in vivo are responsible for reductions in serum T(4) and increases in serum TSH. Male rats were fed control diet or diet containing either 1000 ppm PCN, 250 ppm 3-MC, or 100 ppm PCB for 7 days. Animals were then given [(125)I]T(4) iv, and bile was collected for 2 h. Radiolabeled metabolites in bile were analyzed by reverse-phase HPLC with gamma-detection. PCN, 3-MC, and PCB treatments reduced serum T(4) concentrations by 42, 45, and 73%, respectively, while TSH was only increased by PCN (180%). The biliary excretion of [(125)I]thyronines was increased 103% by PCN, 157% by 3-MC, and 193% by PCB. T(4)-glucuronide was the primary metabolite in bile, accounting for up to 86% of the radiolabeled metabolites in controls. The amount of T(4)-glucuronide excreted in bile was increased 161% and 226% by 3-MC and PCB, respectively, but was only increased 55% by PCN. None of the treatments had any effect on the urinary excretion of [(125)I]T(4). Thus, increased glucuronidation and biliary excretion of T(4) appears likely to be responsible for reductions in serum T(4) produced by microsomal enzyme inducers. Furthermore, increases in T(4) biliary excretion produced by microsomal enzyme inducer treatment are not consistent with changes in TSH. Thus, it can be concluded that differential changes in serum TSH do not stem from differential increases in T(4) biliary excretion.     

慢性阻塞性肺疾病患者血清甲状腺激素水平变化的临床意义

目的 观察慢性阻塞性肺癌病（COPD）患者血清甲状腺激素水平的变化,探讨其临床意义.方法 将兰州军区兰州总医院2012年1月至2013年1月收治的96例COPD患者纳入COPD组,并按病情分为3个亚组,COPD缓解期组（30例）、COPD急性发作无呼吸衰竭组（31例）和COPD急性发作并呼吸衰竭组（35例）;选择同期体检健康者90例作为正常对照组.检测各组甲状腺激素水平.结果 对照组血清总三碘甲状腺原氨酸（TT3）、总四碘甲状腺原氨酸（TT4）、促甲状腺激素（TSH）、游离三碘甲状腺原氨酸（FT3）、游离四碘甲状腺原氨酸（FT4）分别为（1.5±0.5） nmol/L、（96±36） nmol/L、（3.3±1.2） mU/L、（4.4±1.2）pmol/L、（16.6±9.6）pmol/L;COPD组TT3、TT4、TSH、FT3、FT4分别为（0.7±0.3）nmol/L、（66±33）nmol/L、（2.5±1.2） mU/L、（2.1±0.5）pmol/L、（12.1±6.6） pmol/L; COPD组TT4、FT4、TSH、TT3、FT3明显低于正常对照组（P＜0.01或P＜0.05）.COPD缓解期组TT3、T4T、TSH、FT3、FT4分别为（1.13±0.59）nmol/L、（86±28）nmol/L、（3.0 ±0.8） mU/L、（3.2±1.1）pmol/L、（14.3±6.6） pmol/L; COPD急性发作无呼吸衰竭组分别为（0.77±0.45） nmol/L、（66±24） nmol/L、（2.6±0.7） mU/L、（1.9±0.8） pmol/L、（11.3±6.6） pmol/L;COPD急性发作并呼吸衰竭组分别为（0.45±0.24） nmol/L、（44±25）nmol/L、（1.2±0.6）mU/L、（1.5±0.7）pmol/L、（7.9±3.4）pmol/L;COPD急性发作无呼吸衰竭组TT3、FT3明显低于COPD缓解期组（P＜0.05）,TT4、FT4、TSH差异无统计学意义（P＞0.05）,COPD急性发作并呼吸衰竭组TT3、FT3、TT4、FT4、TSH均明显低于COPD缓解组,差异均有统计学意义（均P＜0.01）.结论 甲状腺激素水平可能与COPD患者的病情有密切关系,测定甲状腺激素水平可用于评估COPD患者病情的严重程度,病情越重,甲状腺激素水平下降幅度越大.     

硒酵母联合维生素D对实验性自身免疫甲状腺炎大鼠甲状腺相关激素及抗体的影响 #br#

目的观察硒酵母联合维生素D对实验性自身免疫性甲状腺炎（EAT）大鼠甲状腺相关激素及抗体的作 用。 方法55只雌性SD大鼠,其中45只采用猪甲状腺球蛋白（pTG）致敏+饮用高碘水建立EAT大鼠模型,建模成功 大鼠（40只）采用随机数字表法分为模型组、硒酵母组、维生素D组、联合组,每组10只;其余10只为对照组。加强免 疫4周后,硒酵母组予硒酵母溶液灌胃+腹腔注射生理盐水,维生素D组予生理盐水灌胃+腹腔注射维生素D3注射液, 联合组予硒酵母溶液灌胃+腹腔注射维生素D3注射液,对照组和模型组予生理盐水灌胃+腹腔注射生理盐水。6周 后,比较各组血清游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）、促甲状腺激素（TSH）、甲状腺球蛋白抗体 （TGAb）、甲状腺过氧化物酶抗体（TPOAb）、干扰素-γ（IFN-γ）、白介素（IL）-4、IFN-γ/IL-4;HE染色比较各组甲状腺 组织病理学形态;比较各组甲状腺组织 p38MAPK、环氧合酶-2（COX-2）mRNA 相对表达量及 p38MAPK、pp38MAPK、COX-2蛋白相对表达量。 结果HE染色结果显示,对照组甲状腺滤泡形态正常;模型组甲状腺滤泡结构 破坏,淋巴细胞浸润,间质纤维化;硒酵母组、维生素D组及联合组较模型组均有一定改善,其中联合组改善最为明 显。与模型组比较,硒酵母组、维生素D组、联合组血清FT3、FT4、TSH、TGAb、TPOAb、IFN-γ、IFN-γ/IL-4水平,甲状 腺组织COX-2 mRNA 相对表达量及p-p38MAPK、COX-2蛋白相对表达量均降低（P＜0.05）,血清IL-4水平均升高 （P＜0.05）;与硒酵母组和维生素D组比较,联合组血清FT3、FT4、TSH、TGAb、TPOAb、IFN-γ、IFN-γ/IL-4水平降低 （P＜0.05）,甲状腺组织COX-2 mRNA相对表达量及p-p38MAPK、COX-2蛋白相对表达量均降低,血清IL-4水平升 高（P＜0.05）。 结论硒酵母联合维生素D可有效抑制EAT大鼠甲状腺组织损伤,保护甲状腺组织,其机制可能是通 过抑制MAPK信号通路发挥调控作用。     

新生儿缺氧缺血性脑病生长激素、甲状腺功能变化

目的探讨新生儿缺氧缺血性脑病(NHIE)患儿生长激素及甲状腺功能变化及其与病情轻重的关系。方法应用化学发光免疫分析法测定82例NHIE患儿血生长激素(GH)、三碘甲状腺原氨酸(TT3)、甲状腺素(TT4)、游离T3(FT3)、游离T4(FT4)及促甲状腺(TSH)浓度。结果轻度NHIE仅有TT3降低,中重度NHIETT3、TT4、FT3、FT4、GH均降低,且病情越重,改变越明显,TSH改变不明显。结论NHIE存在着内分泌紊乱,TT3、TT4、FT3、FT4、GH可作为临床判断NHIE病情轻重的参考指标。