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桥本甲状腺炎甲状腺组织Bcl-2、Bax蛋白表达

The studies on expression of Bcl-2 and Bax in Hashimoto's thyroiditis
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摘要 目的 探讨Bcl 2、Bax蛋白在桥本甲状腺炎 (HT)甲状腺组织的表达及其与HT发病机制的关系。方法 采用免疫组化S P法检测 4 1例HT及 10例正常甲状腺组织Bcl 2、Bax表达及分布 ,应用Mias99图像分析系统进行定量分析。结果  (1)HT组甲状腺组织Bcl 2、Bax阳性颗粒面积、平均光密度和积分光密度均显著高于正常组 (P <0 0 1) ,HT组中组织结构破坏较重区域中小滤泡及失去正常滤泡结构的腺上皮Bax表达高于其它腺上皮 ,滤泡结构较完整的区域Bcl 2表达较高 ;(2 )HT甲状腺组织滤泡区Bcl 2阳性颗粒面积、积分光密度与Bax的比值低于正常对照组 (P <0 0 0 1)。结论 HT甲状腺组织Bcl 2、Bax表达失衡导致的细胞凋亡增高可能是HT甲状腺细胞破坏的重要机制之一 ;Bcl Objective To investigate the relationship between the expression of Bcl 2,Bax and the pathological changes in Hashimotos thyroiditis(HT).Methods 41 cases of HT thyroid and 10 cases of normal thyroid specimens were selected.The expression and distribution of Bcl 2 and Bax was detected by using immunohistochemical methods and analyzed by Mias99 pathological image system.Immunohistochemical staining was carried out using S P kit.Results The positive granule area,average light density and total light density of Bcl 2 and Bax in thyriod tissue from HT were higher than those from normal controls( P< 0 01),The thyrocyte in disrupted follicles had an increased Bax expression.The strongly positive Bcl 2 staining was observed in the thyrocyte of intact follicle;The ratio of positive area and total light density of Bcl 1 to Bax in HT thyroid follicle area was lower than in normal thyroid.Conclusion The lost of Bcl 2 and Bax equilibrium may contribute to the pathogenesis of HT.Bcl 2 may be related to the survival of some thyrocyte in HT.
出处 《江苏医药》 CAS CSCD 北大核心 2002年第9期653-655,共3页 Jiangsu Medical Journal
关键词 甲状腺炎 自身免疫性 BCL-2 BAX 免疫组化 Thyroiditis Autoimmune Bcl 2 Bax Immunohistochemical methods
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参考文献3

  • 1Hammond LJ,Lowdell MW,Cerrano PG,et al.Analysis of apoptosis in relation to tissure destruction associated with Hashimoto’s autoimmune thyroiditis[].Journal of Paleopathology.1997
  • 2Barnes DM,Dublin EA,Fisher CJ,et al.Immunohistochemical detection of p53 protein in mammary carcinoma: an important new independent indictor of prognosis[].Human Pathology.1993
  • 3Yin XM,Oltvai ZN,Korsmeyer SJ.BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax[].Nature.1994

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