摘要
目的探究亚甲蓝对糖尿病大鼠视网膜病变的神经保护作用。方法将30只SD大鼠随机分为空白组、对照组和实验组。对照组和实验组采用链脲佐菌素(STZ)腹腔注射构建糖尿病大鼠模型。造模成功6周后,在实验组动物玻璃体内按照[0.2 mg/(kg·d)]剂量注射亚甲蓝,对照组玻璃体内注射等量二甲基亚砜(DMSO),均连续处理7 d。采用ELISA检测大鼠的视网膜超氧化物歧化酶(SOD),8⁃异前列腺素F2α(iPF2α)和白细胞介素1β(IL⁃1β)的水平,Western blot法检测视网膜磷酸化的细胞外信号调节激酶1/2(p⁃ERK1/2)和磷酸化的蛋白激酶B(p⁃AKT)表达,过碘酸希夫(PAS)染色检测视网膜形态变化。结果与空白组大鼠相比,对照组和实验组大鼠中的视网膜SOD活性明显降低,iPF2α和IL⁃1β水平增加,p⁃ERK1/2水平增加、p⁃AKT磷酸化水平降低;与对照组相比,实验组大鼠SOD活性增加,iPF2α和IL⁃1β水平降低,p⁃ERK1/2、p⁃AKT水平明显升高,视网膜层的整体厚度和视网膜神经节细胞的数量显著减少。结论亚甲蓝通过降低视网膜氧化应激和增强ERK1/2和AKT磷酸化改善糖尿病大鼠视网膜病变。
Objective To investigate the neuroprotective effect of methylene blue on diabetic retinopathy in rats.Methods Thirty SD rats were randomly divided into blank,control and experimental groups.The control and experimental groups were induced with diabetes by streptozotocin(STZ)intraperitoneal injection.After 6 weeks of successful modeling,the experimental group received intravitreal injection of methylene blue at a dose of[0.2 mg/(kg·d)],while the control group received an equal amount of dimethyl sulfoxide(DMSO)intravitreal injection,both continuously injected for 7 days.ELISA was used to detect the levels of retinal superoxide dismutase(SOD),8⁃iso⁃prostaglandin F2alpha(iPF2α)and interleukin⁃1β(IL⁃1β)in rats.Western blot analysis was used to detect the expression of retinal extracellular signal⁃regulated kinase 1/2 phosphorylation(p⁃ERK1/2)and phosphorylated protein kinase B(p⁃AKT),and PAS staining was used to detect retinal morphological changes.Results Compared with the blank group rats,the retinal SOD activity in the control and experimental group rats was significantly reduced.iPF2α,IL⁃1βand p⁃ERK1/2 level increased,while p⁃AKT level decreased.Compared with the control group,the SOD activity of the experimental group rats increased.iPF2αand IL⁃1βlevel went down,while p⁃ERK1/2 and p⁃AKT level went up significantly.The overall thickness of the retinal layer and the number of retinal ganglion cells were significantly reduced.Conclusion Methylene blue improves diabetic retinopathy in rats by reducing retinal oxidative stress and enhancing ERK1/2 and AKT phosphorylation.
作者
麦华德
顾申红
符碧薇
纪新博
陈明慧
陈菊明
张云波
林芸芸
刘承红
宋艳玲
MAI Huade;GU Shenhong;FU Biwei;JI Xinbo;CHEN Minghui;CHEN Juming;ZHANG Yunbo;LIN Yunyun;LIU Chenghong;SONG Yanling(Department of General Medicine,The First Affiliated Hospital of Hainan Medical University;Hainan Medical University,Haikou 570102,China)
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2023年第5期423-428,共6页
Chinese Journal of Cellular and Molecular Immunology
基金
海南省自然科学基金(821RC689)。
