糖尿病大鼠视网膜中缺氧诱导因子-1α和血管内皮生长因子表达的研究  被引量:15

Expression of hypoxia-inducible factor-1α and vascular endothelial growth factor in the retina of diabetic rats

在线阅读下载全文

作  者:徐国兴[1] 许建斌[1] 胡建章[1] 

机构地区:[1]福建医科大学附属第一医院福建省眼科研究所,中国福建省福州市350005

出  处:《国际眼科杂志》2008年第3期487-490,共4页International Eye Science

基  金:中国卫生部攻关课题基金资助项目(No.WKJ2005-2-013);中国福建省自然科学科研课题基金资助项目(No.C0510015);中国福建省教育厅科研基金资助项目(No.JB05244)~~

摘  要:目的:检测缺氧诱导因子-1α(HIF-1α)与血管内皮生长因子(VEGF)在糖尿病大鼠视网膜中的表达,探讨其在糖尿病视网膜病变(DR)发生发展中的作用。方法:SD大鼠120只随机分为对照组与DR组,DR组采用链脲佐菌素(STZ)一次性建立糖尿病模型。应用免疫组化SP法和RT-PCR技术分别于1,3,6mo检测视网膜中HIF-1α与VEGF蛋白及其mRNA的表达变化。结果:HIF-1α与VEGF蛋白及其mRNA在对照组视网膜中不表达,在DR组中呈进行性表达增强(P<0.05);DR组中HIF-1α与VEGF的表达呈正相关(r=0.605,P<0.05)。结论:DR视网膜中HIF-1α与VEGF表达增强,与DR的发生发展密切相关。AIM: To detect the expression of hypoxia-inducible factor- 1α (HIF-1α) and vascu1αr endothelial growth factor (VEGF) in the retina of diabetic rats, and to investigate their roles in the pathogenesis of diabetic retinopathy (DR). METHODS: One hundred and twenty SD rats were randomly divided into two groups: DR group and control group. Diabetes was induced by streptozotocin (STZ) intraperitoneal injection in DR group. The techniques of immunohistochemistry and reverse transcription poly- merase chain reaction (RT-PCR) were used to examine the expression of HIF-1α, VEGF protein and mRNA in retina respectively at 1,3,6 months after STZ injection. RESULTS. The results of immunohistochemical technique and RT-PCR showed that the expression of HIF-1α, VEGF protein and mRNA in retina were not found in control group, but were found gradually increased in DR group ( P 〈 0.05). There was a positive corre1αtion between the expression of HIF-1α and that of VEGF(r=0.605,P〈0.05). CONCLUSION, HIF-1α may regu1αte the expression of VEGF, and both are involved in the pathogenesis of DR.

关 键 词:糖尿病视网膜病变 缺氧诱导因子-1Α 血管内皮生长因子 

分 类 号:R587.2[医药卫生—内分泌] R735.34[医药卫生—内科学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象