STZ诱导的糖尿病鼠视网膜β-连环蛋白表达上调

Increased expression of β-catenin in the streptozotocin-induced diabetic rat retina

目的:探讨链脲霉素(Streptozotocin,STZ)诱导的糖尿病鼠视网膜β-连环蛋白(β-catenin)表达以及与早期糖尿病视网膜病变发展的可能关系。方法:建立STZ诱导的糖尿病大鼠模型,用伊文思蓝检测视网膜血管的渗透性;免疫组织化学和Westernblot方法检测糖尿病鼠视网膜及胰蛋白酶消化的视网膜微血管β-连环蛋白的表达情况。结果:糖尿病诱导4、8和12wk后视网膜血管渗透性分别增加68%、91%和125(%P<0.005)。免疫组化分析证实对照组视网膜β-连环蛋白主要表达在视网膜光感受器、外网状层、内网状层、神经节细胞层、内界膜及视网膜微血管内皮细胞和周细胞。STZ诱导糖尿病大鼠12wk后,视网膜及视网膜微血管β-连环蛋白表达显著增加。West-ernblot分析证明随着糖尿病视网膜病变的发展,视网膜β-连环蛋白表达显著增加。结论:STZ诱导的糖尿病视网膜β-连环蛋白的表达增加,提示β-连环蛋白可能参与早期糖尿病视网膜病变的发生。

AIM： To study the expression of β -catenin in streptozotodn （STZ）-induced diabetic rat retina and the possible relevance of β -catenin in the early stage of STZ-induced diabetic retinopathy. METHODS： Vascular permeability was quantified by measuring albumin leakage from blood vessels into the retina using the Evans blue method. The model of STZ-induced diabetic rat was set up. β -catenin expression was measured in both normal and STZ-induced diabetic rat retinas and retinal microvessel using immunohistochemistry and Western blot analysis. RESULTS： Retinal vascular permeability was increased by 68%, 91% and 125% in the 4-, 8- and 12-weak diabetic retinas, respectively, compared with that in the controls （P 〈 0.005）. Tmmunohistochemistry showed the expression of β-catanin was detected and localized to the photoceptor, outer plexiform layer, inner plexiform layer, ganglion cell layer, internal limiting membrane and microvessel of rat retinas. However, the expression of β -catenin was significantly increased in STZ-induced diabetic rat retinas with the progression of diabetes. CONCLUSION： The increased expression of β -catenin in the retinas of STZ-induced diabetic rat may reflect that β-catanin participates in the development of diabetic retinopathy.