摘要
目的:研究莱菔硫烷(SF)对糖尿病大鼠视网膜神经细胞的保护效应,并初步探讨其作用机制。方法:通过一次性腹腔注射链脲佐菌素的方法制备糖尿病大鼠模型;通过测定活性氧簇(ROS)的生成、TUNEL法检测视网膜细胞的凋亡和计数存活的视网膜神经节细胞(RGCs)等方法作为指标观察SF对糖尿病大鼠视网膜神经细胞的保护效应;以免疫组织化学染色和Western blot法检测视网膜核因子E2相关因子2(Nrf2)的核转移和血红素加氧酶1(HO-1)的表达变化。结果:SF能抑制糖尿病大鼠视网膜ROS的生成,抑制视网膜神经细胞的凋亡并增加糖尿病大鼠视网膜RGCs的存活数量;同时SF还可促进Nrf2的激活及HO-1蛋白表达;使用HO-1抑制剂锌原卟啉可明显减弱SF对糖尿病大鼠视网膜RGCs凋亡的抑制作用。结论:SF可能通过激活Nrf2/HO-1抗氧化通路改善糖尿病大鼠视网膜氧化应激状态,减少视网膜神经细胞凋亡,减轻糖尿病大鼠的视网膜损伤。
AIM：To clarify whether sulforaphane（SF） has protective effects on retina neuronal cells in diabetic rats and to identify the related mechanisms involved in this process.METHODS：The diabetic rat model was induced by single intraperitoneal injection of streptozotocin（STZ）.The protective effects of SF were evaluated by measuring the generation of reactive oxygen species（ROS）,detecting apoptosis of retina neuronal cells with TUNEL staining and counting the survival retinal ganglion cells（RGCs）.The nuclear translocation of nuclear factor E2-related factor 2（Nrf2） and the protein expression of heme oxygenase-1（HO-1） were examined by immunofluorescence analysis and Western blot.RESULTS：SF treatment significantly attenuated ROS generation,decreased the apoptosis of retina neuronal cells and increased the numbers of survival RGCs in the diabetic rats.Meanwhile,SF significantly increased the nuclear accumulation of Nrf2 and the protein level of HO-1 in the retinas of diabetic rats.However,HO-1 inhibitor,protoporphyrin IX zinc（II）diminished the inhibitory effects of SF on RGCs apoptosis.CONCLUSION：SF partially exerts the beneficial neuroprotective effects via the activation of the Nrf2/HO-1 antioxidant pathway,therefore alleviating retinal oxidative stress and decreasing the apoptosis of retina neuronal cells.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2017年第11期1938-1944,共7页
Chinese Journal of Pathophysiology
基金
山东省自然科学基金资助项目(No.BS2015YY036
No.ZR2014CM038
No.ZR2013HL009)
