J4 ›› 2010, Vol. 36 ›› Issue (5): 854-857.

• 基础研究 • 上一篇    下一篇

甲状腺激素缺乏对不同发育时期大鼠脑组织氧化应激指标的影响

张洪梅1, 苏青1, 罗敏2   

  1. 1.上海交通大学医学院附属新华医院内分泌科|上海 200092;2. 上海交通大学医学院附属瑞金医院内分泌及代谢研究所|上海 200025
  • 收稿日期:2010-02-08 出版日期:2010-09-28 发布日期:2010-09-28
  • 通讯作者: 苏 青(Tel: 021-65790000-7530,E-mail:suqingxinhua@yahoo.com.cn) E-mail:suqingxinhua@yahoo.com.cn
  • 作者简介:张洪梅(1975-)|女|吉林省长春市人|主治医师|在读医学博士|主要从事内分泌代谢病发病机制研究。
  • 基金资助:

    国家自然科学基金资助课题(30200127)

Effect of thyroid hormone deficiency on oxidative stress parameters

 ZHANG Hong-Mei1, SU Qing1, LUO Min2   

  1. 1.Department of Endocrinology,Xinhua Hospital,School of Medcal Sciences,Shanghai Jiaotong University,Shanghai 200092,China;2.Institute of Endocrinology and Metablism,Ruijin Hospital,School of Medical Sciences,Shanghai Jiaotong University,Shanghai 200025,China
  • Received:2010-02-08 Online:2010-09-28 Published:2010-09-28

摘要:

目的:研究甲状腺激素缺乏对不同发育时期大鼠脑组织丙二醛(MDA)、总抗氧化力(TAC)及超氧化物歧化酶(SOD)的影响,探讨甲状腺激素缺乏影响鼠脑发育的机制。方法:实验组以丙基硫氧嘧啶溶液灌胃孕鼠制造大鼠围产期甲状腺激素缺乏模型,收集出生后7、14和21 d的仔鼠血清和脑组织,测定血清游离三碘甲状原氨酸及甲状腺素(FT3 、FT4)水平,脑组织匀浆后检测MDA、TAC及SOD的水平。正常孕鼠所产的年龄匹配仔鼠作为对照组,同样测定上述指标。结果:21 d实验组仔鼠脑组织MDA水平高于正常对照组[(14.63±3.44)  μmol/g vs  (10.52±2.32)  μmol/g,P<0.05];TAC水平高于正常对照组[(0.051±0.006) mmol/g- vs  (0.042±0.003) mmol/g,P<0.05];SOD活性高于正常对照组[(79.63±10.10)  μmol?min-1/g  vs  (63.51±8.35) μmol/min/g,P<0.05]。实验组与对照组7 d和14 d的标本MDA水平、TAC水平及SOD活性比较差异无显著性[7 d MDA:(11.20±2.39)  μmol/g  vs  (12.29±1.79)  μmol/g,P>0.05;14 d MDA: (13.07±3.16)  μmol/g  vs  (12.98±2.93)  μmol/g,P>0.05;7 d TAC:(0.046±0.006) mmol/g- vs  (0.047±0.004) mmol/g,P>0.05;14 d TAC:(0.042±0.007) mmol/g  vs  (0.046±0.007) mmol/g,P>0.05;7 d SOD:(66.34±11.20)  μmol/min/g  vs  (65.49±7.52)  μmol/min/g,P>0.05;14 d SOD:(67.53±12.01)  μmol/min/g  vs  (64.57±8.28)  μmol/min/g,P>0.05]。结论:大鼠脑发育期甲状腺激素缺乏可引起脑组织MDA水平、TAC水平及SOD活性的改变,这可能参与了甲状腺功能减退性脑损伤的发生。

关键词: 甲状腺激素缺乏;丙二醛;总抗氧化力;超氧化物歧化酶;脑发育

Abstract:

Abstract:Objective
To study the effect of thyroid hormone deficiency on malonaldehyde (MDA) and total antioxidative capacity (TAC) and superoxide dismutase (SOD) levels in different developing stages of rat brain and  further explore the mechanism of impaired brain development caused by thyroid hormone deficiency. Methods Perinatal hypothyroidism was induced by administering propylthiouracil ( PTU) solution to the dams by gavage (2 % PTU 1. 5 mL/d) beginning on embryonic day 15. The blood samples of  pups in different developing stages(7,14,21 d) were collected to measure serum FT3 and FT4 levels. And the brain tissues were collected to measure MDA,TAC and SOD levels in brain homogenate. Age matched controls were pups from normal dams without administering propylthiouracil ( PTU) solution. Results Compared with age matched controls,the MDA and TAC and SOD levels were increased in hypothyroid group of 21 d pups(MDA:14.63 μmol/g/±3.44  μmol/g  vs  10.52 μmol/g ±2.32  μmol/g,P<0.05;TAC:0.051 mmol/g±0.006 mmol/g  vs  0.042 mmol/g±0.003 mmol/g,P<0.05;SOD:79.63 μmol/min/g±10.10  μmol/min/g   vs  63.51 μmol/min/g±8.35 μmol/min/g,P<0.05),but for the 7 d and 14 d pups,ther
e were no differences between two groups (7 d MDA:11.20 μmol/g±2.39  μmol/g vs  12.29 μmol/g±1.79  μmol/g,P>0.05;14 d MDA:13.07 μmol/g±3.16  μmol/g  vs  12.98 μmol/±2.93  μmol/g,P>0.05;7 d TAC:0.046 mmol/g  ±0.006 mmol/g vs  0.047 mmol /g  ±0.004 mmol/g,P>0.05;14 d TAC:0.042 mmol/g  ±0.007 mmol/g  vs  0.046 mmol/g ±0.007 mmol/g,P>0.05;7 d SOD:66.34 μmol?min-1/g ±11.20  μmol/min/g  vs  65.49 μmol/min/g±7.52  μmol/min/g,P>0.05;14 d SOD:67.53  μmol/min/g±12.01  μmol/min/g  vs  64.57  μmol/min/g±8.28  μmol/min/g/,P>0.05). Conclusion Thyroid hormone deficiency during rat brain development may cause the changes of MDA,TAC and SOD levels and this may be related to brain damage caused by thyroid hormone deficiency.

Key words: thyroid hormone deficiency;malondialdehyde;total antioxidant capacity;superoxide dismutase;brain development

中图分类号: 

  • R363