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Graves病内源性硫化氢的水平变化意义及其生成机制

汪新宇 梁倩 姚伟力 欧慧婷 吕凌波

山东医药2018,Vol.58Issue(13):21-23,3.
山东医药2018,Vol.58Issue(13):21-23,3.DOI:10.3969/j.issn.1002-266X.2018.13.006

Graves病内源性硫化氢的水平变化意义及其生成机制

Changes of endogenous gas hydrogen sulfide levels and genesis mechanism in Graves'disease

汪新宇 1梁倩 2姚伟力 1欧慧婷 2吕凌波1

作者信息

  • 1. 深圳市第二人民医院,深圳518037
  • 2. 深圳大学医学部
  • 折叠

摘要

Abstract

Objective To investigate the level and role of endogenous gaseous hydrogen sulfide (H2S) in patientswith diffuse toxic goiter (Graves disease,GD),and to explore its generative mechanism.Methods The serum of 20 GD patients without treatment (untreated group),20 patients with remission of GD (treatment remission group,GD) and 20 patients with thyroid nodules (control group) was collected,and we measured the concentrations of H2S by spectrophotometry.At the same time,8 patients in each group were selected and their thyroid tissues were taken.RT-PCR-was used to detect the mRNA levels of cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE).Results Compared with the control group,the concentration of H2S decreased in the untreated group (P < 0.05);the concentration of H2S increased in the treatment remission group as compared with that of the untreated group (P < 0.05).CBS mRNA expression was found in the control group,but it decreased in the thyroid tissues of the untreated group.The CBS mRNA expression increased in the thyroid tissues of the treatment remission group (all P < 0.05),but CSE mRNA was not expressed.Conclusions The level of endogenous H2S in patients with GD decreases,which may play an anti-inflammatory role in the pathogenesis of GD.The enzyme that catalyzes the synthesis of H2S in thyroid tissues is mainly CBS,not CSE.

关键词

毒性弥漫性甲状腺肿/硫化氢/胱硫醚-β合成酶/胱硫醚-γ-裂解酶

Key words

toxic diffuse goiter/endogenous gas hydrogen sulfide/cystathionine-β-synthase/cystathionine-γ-lyase

分类

医药卫生

引用本文复制引用

汪新宇,梁倩,姚伟力,欧慧婷,吕凌波..Graves病内源性硫化氢的水平变化意义及其生成机制[J].山东医药,2018,58(13):21-23,3.

基金项目

深圳市科技计划项目(JCY20150330102720141). (JCY20150330102720141)

山东医药

OACSTPCD

1002-266X

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