GRP94、EIF2α在原发型闭角性青光眼小梁中的作用研究  

Role of GRP94 and EIF2α in trabecular bone of primary angle-closure glaucoma patients

作　　者：滕兴波 曹智[1] 孙海霞 刘宪金 杨伟舟 朱艳[2] 朱玉广[2] TENG Xingbo;CAO Zhi;SUN Haixia;LIU Xianjin;YANGa Weizhou;ZHU Yan;ZHU Yuguang(Department of Ophthalmology, Weifang Medical University, Weifang 261053, Shandong, China;Eye Center of Affiliated Hospital of Weifang Medical University, Weifang 261031, Shandong, China)

机构地区：[1]潍坊医学院眼科教研室,山东潍坊261053 [2]潍坊医学院附属医院眼科,山东潍坊261031

出　　处：《山东大学耳鼻喉眼学报》2019年第2期115-118,共4页Journal of Otolaryngology and Ophthalmology of Shandong University

基　　金：山东省卫生厅科技计划资助项目(2015WS0047)

摘　　要：目的通过检测内质网应激的相关因子GRP94、EIF2α在原发性慢性闭角型青光眼(PCACG)患者小梁组织中的表达,研究内质网应激在PCACG小梁组织氧化损伤中的作用,探讨PCACG的发病机制。方法分别用HE染色法观察实验组及对照组小梁组织镜下显微形态的变化、免疫组化法测定实验组及对照组小梁组织中内质网应激相关因子GRP94、 EIF2α的表达水平。结果 HE染色显示,PCACG患者小梁组织排列不规则,小梁网眼窄小,Schlemm管腔变窄且不规则。免疫组化结果显示,对照组的小梁网组织GRP94、EIF2α少量表达,实验组小梁组织中GRP94、EIF2α的表达明显增加,差异均具有统计学意义(P<0.05)。结论 PCACG患者小梁组织中存在内质网应激,内质网应激EIF2α通道参与了小梁组织的氧化损伤,促进了眼内压的升高。Objective The aim of this study was to investigate the role of endoplasmic reticulum stress in trabecular tissue of patients with chronic primary angle-closure glaucoma (PCACG) and to explore its role in the pathogenesis of PCACG. Methods Hematoxylin and eosin (H&E) staining was used to observe changes in the microscopic morphology of trabeculae. Expression of the endoplasmic reticulum stress-related factors, GRP94 and EIF2α, in trabecular tissues, was determined by immunohistochemistry. Results staining showed altered morphology of trabecular tissues, such as the narrow trabeculae and narrow lumen and irregular pigmentation of Schlemm's canal. Immunohistochemistry results showed that GRP94 and EIF2α were expressed in the trabecular tissue of the control group and their expression increased significantly in the experimental groups (P<0.05). Conclusion These results show that endoplasmic reticulum stress occurs in the trabecular tissue of PCACG patients. The EIF2α signaling pathway may participate in the oxidative damages of trabecular tissue and promote an increase in intraocular pressure.

关 键 词：GRP94 EIF2Α 内质网应激 原发性慢性闭角型青光眼 

分 类 号：R775.1[医药卫生—眼科]