内源性硫化氢在糖尿病肾病大鼠肾组织中表达

陈燊; 黄雯; 张红; 杨敏; 张梅

doi:10.3969/j.issn.1671-4091.2010.08.007

中国血液净化 >

2010 , Vol. 9 >Issue 8: 433 - 435

DOI: https://doi.org/10.3969/j.issn.1671-4091.2010.08.007

临床研究

内源性硫化氢在糖尿病肾病大鼠肾组织中表达

陈燊 ,
黄雯 ,
张红 ,
杨敏 ,
张梅

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北京同仁医院

收稿日期: 2009-12-30

修回日期: 1900-01-01

网络出版日期: 2010-08-12

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The expression of endogenous H2S in the kidney of diabetic nephropathic rats

The expression of endogenous HS in the kidney of diabetic nephropathic rats

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Department of Nephrology, Beijing Tong Ren Hospital, Capital Medical University, Beijing 100730, China

Received date: 2009-12-30

Revised date: 1900-01-01

Online published: 2010-08-12

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摘要

【摘要】目的探讨内源性硫化氢(H2S)在糖尿病肾病大鼠肾脏表达和作用。方法比较对照组、糖尿病肾病组(DN组)和外源性H2S干预组(H2S组)大鼠肾组织中H2S合酶活性、胱硫醚-裂解酶(cystathionine -、胱硫醚-合成酶(cystathionine-，CBS)mRNA的含量以及肾脏病理改变。结果 DN组大鼠肾脏中H2S生成减少、CSE mRNA含量降低(P＜0.01)；三组大鼠CBS mRNA差异无统计学意义(P＞0.05)，H2S组大鼠肾脏病理改变较DN组大鼠减轻。结论 DN组大鼠肾脏内源性H2S生成减少和CSE表达降低有关。给予外源性H2S可减缓肾脏病变进展。

关键词： 硫化氢; 糖尿病肾病; 胱硫醚-合成酶; 胱硫醚-裂解酶

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陈燊 , 黄雯 , 张红 , 杨敏 , 张梅 . 内源性硫化氢在糖尿病肾病大鼠肾组织中表达[J]. 中国血液净化, 2010 , 9(8) : 433 -435 . DOI: 10.3969/j.issn.1671-4091.2010.08.007

Abstract

【Abstract】Objective The aim of the study was to explore the role and expression of H2S in the kidney of diabetic nephropathic rats. Methods Glomerular pathology, H2S generating enzyme activity in kidney, and relative amount of cystathionine -γ-lyase (CSE) mRNA and cystathionine-β-synthase (CBS) mRNA, the mRNAs of the two endogenous H2S synthesis enzymes, in kidney were compared among diabetic nephropathic group (DN group), DN+ NaHS group (H2S group) and control group. Results H2S generating enzyme activity and the relative amount of CSE mRNA were significantly decreased in kidney in DN group (p<0.01), but CBS mRNA was similar in the 3 groups (p>0.05). Glomerular pathology was less severe in H2S group than in DN group. Conclusion The decrease of endogenous H2S in DN group may result from the lower expression of CSE in the kidney. Exogenous H2S treatment may delay the progression of diabetic nephropathy.

Key words： Diabetic nephropathy; Cystathionine-β-synthase; Cystathionine-γ-lyase

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