摘要
目的:探讨17β-雌二醇对高氧诱导的视网膜神经节细胞层(retinal ganglion cell layer,RGCL)细胞凋亡的保护作用并探讨其机制。方法:7天龄SD大鼠48只随机分为4组,每组l2只,分为正常对照组、单纯高氧组、雌二醇高氧组及溶媒高氧组,单纯高氧组于氧浓度750mL/L的容器内饲养5d,再置正常空气下饲养至17天龄,雌二醇高氧组饲养方法同单纯给氧组,在大鼠7~17天龄间每日皮下注射17β-雌二醇(E2,植物油稀释,配制浓度为2g/L)0.5μL/d,溶媒高氧组饲养方法同雌二醇高氧组,药物改为相同体积植物油。眼球切片并行TUNEL染色和HE染色,观察4组RGCL的细胞形态,免疫组化染色观察诱生型一氧化氮合酶(iNOS)的表达。结果:4组小鼠RGCL均见部分细胞凋亡及TUNEL染色阳性,单纯高氧组的TUNEL阳性细胞数显著多于正常组,雌二醇高氧组显著少于单纯给氧组和溶媒高氧组。视网膜免疫组织化学检测雌二醇干预组iNOS与单纯高氧组有统计学差异(P<0.05),单纯高氧组与正常对照组有统计学差异(P<0.05)。结论:17β-雌二醇可较高氧诱导的视网膜细胞凋亡少,机制可能与NO相关。
AIM:To explore the protective effects of 17β-estradiol on the cell apoptosis in retinal ganglion cell layer which is induced by hyperxia. METHODS: Forty-eitht 7-day-old SD rats were divided into four groups:normal group, high oxygen group, 17β- estradiol treatment group and vegetable oil treatment group. Rats of the high oxygen group were put into the environment exposed to 750mL/L oxygen for 5 days and backed to room air for another 5 days to establish the oxygen- induced retinopathy (OIR) model. The treatment group were given 17β-estradiol by injection with the dose of 0.5μ L/d(2g/L) before exposed to 750mL/L oxygen. The vegetable oil treatment group is similar to 17β-estradiol treatment group, but the medicine changed . Ocular cross-sections were prepared for staining of HE and eyeball slicing parallel TUNEL staining. To observe the cell morphology of 4 groups RGCL. And the expression of inducible nitric oxide synthase (iNOS) of immunohis-tochemical staining. RESULTS: Part of apoptosis and positive TUNEL staining in 4 groups of mice. The number of TUNEL-positive cells in pure oxygen exposure significantly more than the normal group, estradiol high-oxygen group was significantly less than pure oxygen group and solvent group hyperoxia. Retinal immunohistochemistry iNOS estradiol intervention group with a simple high-oxygen group has significant difference ( P〈 0.05), hyperoxia group and normal control group has significant difference ( P〈 0.05). CONCLUSION. 17β-estradiol have protective effects on cell apoptosi caused by hyperxia in retinal ganglion cell layer. The mechanism may relate with NO.
出处
《国际眼科杂志》
CAS
2009年第3期447-450,共4页
International Eye Science