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高碘增加大鼠甲状腺细胞TRAIL表达 被引量:3

Iodine excess induces TRAIL expression of thyrocytes in rats
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摘要 建立雌性SD大鼠实验性自身免疫性甲状腺炎(EAT)模型,饲以高碘饮食,正常对照组、正常高碘组、EAT对照组和EAT高碘组FT_3、FT_4依次增高(P<0.05或P<0.01)。半定量RT-PCR、Western印迹结果显示肿瘤坏死因子相关凋亡诱导配体(TRAIL)在各组大鼠甲状腺中均有表达,其表达在正常对照组、正常高碘组、EAT对照组、EAT高碘组依次增高(P<0.01),高碘可能通过增加TRAIL表达诱导甲状腺细胞过度凋亡,进而影响其功能及病理学改变。 Experimental autoimmune thymiditis (EAT) animal model was established in female SD rats fed with high iodine diet. The concentrations of FT3 and FT4 were increasing in order of normal control group, iodine excess control group, EAT control group and EAT iodine excess group ( P 〈 0.05 or P 〈 0.01 ), Semiquantitative RT-PCR and Western-blotting results showed that the expression of TNF-related apoptesis-inducing ligand (TRAIL) existed in thyrocytes of each group, while the expression was increasing in order of normal control group, iodine excess control group, EAT control group and EAT iodine excess group ( P 〈 0.01 ), The results suggested that high iodine diet might induce thyrocytes' apoptosis by increasing the expression of TRAIL and hence influencing functional and pathologic changes of thyroid grand.
出处 《中华内分泌代谢杂志》 CAS CSCD 北大核心 2006年第6期534-536,共3页 Chinese Journal of Endocrinology and Metabolism
关键词 肿瘤坏死因子相关凋亡诱导配体 甲状腺炎 自身免疫性 Iodine Tumor necrosis factor-related apoptosis-inducing ligand Thyroiditis, autoimmune
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