摘要
目的探讨内源性硫化氢(H2S)在Graves病(GD)患者中的水平变化及其作用,并初步探索其生成机制。方法选择未经药物治疗GD患者20例(未治疗组)、药物治疗后缓解GD患者20例(治疗缓解组)和单纯性甲状腺结节患者20例(对照组),通过分光光度计法测定血清中H2S浓度;同时每组中选取8例患者,取其甲状腺组织,采用RT-PCR技术检测胱硫醚-β-合成酶(CBS)mRNA、胱硫醚-γ-裂解酶(CSE)mRNA水平。结果未治疗组与对照组相比,血清中H2S浓度下降(P<0.05),治疗缓解组与未治疗组相比,血清中H2S浓度增加(P<0.05)。对照组中可见CBS mRNA表达,而未治疗组甲状腺组织中可见CBS mRNA减少,治疗缓解组甲状腺组织中CBS mRNA增加(P均<0.05),未见CSE mRNA表达。结论 GD患者内源性H2S水平降低,其在GD发病过程中可能起着抑炎作用,在甲状腺组织中催化H2S合成的酶主要是CBS,而不是CSE。
Objective To investigate the level and role of endogenous gaseous hydrogen sulfide( H2 S) in patients with 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 H2 S 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 H2 S decreased in the untreated group( P〈0. 05); the concentration of H2 S 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 H2 S in patients with GD decreases,which may play an anti-inflammatory role in the pathogenesis of GD. The enzyme that catalyzes the synthesis of H2 S in thyroid tissues is mainly CBS,not CSE.
作者
汪新宇
梁倩
姚伟力
欧慧婷
吕凌波
WANG Xinyu1, LIANG Qian, YAO Weili, OU Huiting, LYU Lingbo(1 Department of Endocrinology, The Second People's Hospital of Shenzhen, Shenzhen 518037, Chin)
出处
《山东医药》
CAS
2018年第13期21-23,共3页
Shandong Medical Journal
基金
深圳市科技计划项目(JCY20150330102720141)