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Explore the molecular mechanism of angle-closure glaucoma in elderly patients induced telomere shortening of retinal ganglion cells through oxidative stress

机译:探讨老年闭角型青光眼氧化应激诱导视网膜神经节细胞端粒缩短的分子机制

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摘要

Senile glaucoma is a common ophthalmological disease in the elderly. It is a disease of visual papillary perfusion caused by elevated intraocular pressure, complicated by visual dysfunction. Glaucoma can cause serious damage to the normal vision of the elderly. Therefore, exploring the related molecular mechanisms of glaucoma is of great significance to the diagnosis and treatment of glaucoma. This is an exploratory study. Establish a mouse model and conduct experimental groupings. After one week of adaptive feeding, the mice were intraperitoneally injected with an anesthetic mixture: ketamine + xylazine. Then the mice were sacrificed by neck dissection, and the eyeball tissues were immediately dissected. HE staining was used to analyze the histopathological characteristics of the retina of each group of mice. MitoSOX fluorescent probe was used to analyze the content of ROS in retinal tissue. The ELISA analysis was used to detect the activation of beta-galactosidase for the aging characteristics of retinal ganglion cells in retinal tissues. Immunohistochemistry experiments were used to analyze the expression of telomerase TERT in retinal tissues. Western blot analysis was used to determine the expression of proteins POT1, TERF1, TERF2, and TINF2 in retinal tissues. The HE staining experiment showed that the damage of retinal tissue decreased from group Glaucoma to group Old, group Old to group Young. The experimental results of MitoSOX fluorescent probe show that ROS content is positively correlated with the degree of tissue damage. ELISA analysis results showed that the expression trend of beta-galactosidase was the same as the ROS content. The protein expression levels related to telomere protection (TRET, POT1, TREF1, TREF2 and TINF2) all increased from group Glaucoma to group Old, group Old to group Young. The increase in ROS content, the decrease in telomere protection-related protein expression (telomere shortening) induced by ROS, and the increase of the expression of beta-galactosidase, are all potential molecular mechanisms for the occurrence of angle-closure glaucoma in elderly patients.
机译:老年性青光眼是老年人常见的眼科疾病。它是一种由眼压升高引起的视觉状灌注疾病,并发视觉功能障碍。青光眼会对老年人的正常视力造成严重损害。因此,探索青光眼的相关分子机制对青光眼的诊疗具有重要意义。这是一项探索性研究。建立小鼠模型并进行实验分组。适应性喂养一周后,小鼠腹膜内注射麻醉剂混合物:氯胺酮+甲苯噻嗪。然后通过颈部解剖处死小鼠,并立即解剖眼球组织。HE染色分析各组小鼠视网膜的组织病理学特征。采用MitoSOX荧光探针分析视网膜组织中ROS的含量。ELISA法检测β-半乳糖苷酶激活对视网膜组织中视网膜神经节细胞衰老特性的影响。采用免疫组化实验分析端粒酶TERT在视网膜组织中的表达。Western blot分析检测视网膜组织中POT1、TERF1、TERF2和TINF2蛋白的表达。HE染色实验显示,视网膜组织损伤从青光眼组到老年组,老年组到年轻组均呈下降趋势。MitoSOX荧光探针的实验结果表明,ROS含量与组织损伤程度呈正相关。ELISA分析结果显示,β-半乳糖苷酶的表达趋势与ROS含量相同。与端粒保护相关的蛋白表达水平(TRET、POT1、TREF1、TREF2和TINF2)均从青光眼组到老年组,老年组到年轻组。ROS含量的增加、ROS诱导的端粒保护相关蛋白表达(端粒缩短)的降低以及β-半乳糖苷酶表达的增加,都是老年患者闭角型青光眼发生的潜在分子机制。

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