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短期碘缺乏和碘过量对大鼠甲状腺细胞凋亡和增殖的影响
引用本文:林来祥,孙毅娜,张璐,阎玉芹,陈祖培.短期碘缺乏和碘过量对大鼠甲状腺细胞凋亡和增殖的影响[J].环境与健康杂志,2007,24(8):571-574.
作者姓名:林来祥  孙毅娜  张璐  阎玉芹  陈祖培
作者单位:天津医科大学内分泌研究所,卫生部激素与发育重点实验室,天津,300070
摘    要:目的 检测碘缺乏和碘过量对甲状腺细胞凋亡和增殖的影响,以期为防治碘致性甲状腺疾病提供理论依据.方法 将断乳后1个月Wistar大鼠随机分为低碘组、适碘组、5、10、50倍碘组,各组大鼠分别以0.6、6.15、30.75、61.5、307.5μg/d进行饮水染毒.在实验第7、14、28天,处死动物并分离甲状腺.采用RT-PCR检测细胞凋亡相关基因fas、fasL mRNA表达,免疫组化方法检测细胞Fas、FasL蛋白及增殖细胞核抗原(PCNA)的表达,末端标记法(TUNEL)检测凋亡细胞.结果 与适碘组比较,各时间段低碘组大鼠甲状腺fas和fasL mRNA的表达均无明显变化,5、10、50倍碘组有随碘摄入量增加而增强的趋势.Fas和FasL蛋白在各时间段,低碘组和适碘组稳定的表达为阴性或弱阳性,5、10、50倍碘组阳性强度随碘摄入量和摄入时间增加而增强.在各时间段,与适碘组比较,低碘组大鼠甲状腺PCNA表达阳性细胞率较高;5、10、50倍碘组无显著变化.各组大鼠各时段均未发现阳性凋亡细胞.结论 短期碘缺乏未引起细胞凋亡,但促进细胞增殖;短期碘过量对甲状腺细胞凋亡和增殖活性均无影响;机体对碘过量有较强的适应能力.

关 键 词:  甲状腺  凋亡  大鼠
文章编号:1001-5914(2007)08-0571-04
修稿时间:2007年3月15日

Effects of Different Iodine Intake on Apoptosis and Proliferation of Rats Thyroid Cells
LIN Lai-xiang,SUN Yi-na,ZHANG Lu,et al..Effects of Different Iodine Intake on Apoptosis and Proliferation of Rats Thyroid Cells[J].Journal of Environment and Health,2007,24(8):571-574.
Authors:LIN Lai-xiang  SUN Yi-na  ZHANG Lu  
Institution:LIN Lai-xiang,SUN Yi-na,ZHANG Lu,et al. Institute of Endocrinology,Tianjin Medical University,Tianjin 300070,China
Abstract:Objective To explore the effects of iodine on apoptosis and proliferation of the thyroid cells. Methods Wistar rats of one month wean were randomly divided into five groups(low iodine-LI, normal iodine-NI, fivefold high iodine-5 HI, tenfold high iodine-10 HI, fiftyfold high iodine-50 HI), and fed on water containing different concentration of iodine. All groups got prospective iodine intake, that is 0.6, 6.15, 30.75, 61.5, and 307.5 mg/d. After 7 days, 14 days, 28 days, the rats were sacrificed. The proliferation, apoptosis, and apoptosis related genes expression in the thyroid cells were determined by TUNEL, immunohistochemistry and RT-PCR. Results As for short-term of iodine deficiency, no significant change was seen in the mRNA expression of fas and fasL genes, while in the iodine excess groups,the expreesion showed an up-regulation trend as iodine intake increased. Fas and FasL proteins expressions were consistent in LI and NI groups and all of them were negative or weak positive. In the HI groups the stain density increased with iodine intake and treatmnet period increased. Expression of PCNA was enhanced by short-term iodine deficiency, but not by short-term iodine excess. Apoptosis was not observed in all groups. Conclusion Both short-term iodine deficiency and iodine excess have no obvious effects on thyrocytes apoptosis. Proliferation can be induced by short-term iodine deficiency, not by iodine excess. Wistar rats present a strong tolerance to long-term iodine excess.
Keywords:Iodine  Thyroid gland  Apoptosis  Rats
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