山东大学耳鼻喉眼学报 ›› 2019, Vol. 33 ›› Issue (2): 115-118.doi: 10.6040/j.issn.1673-3770.0.2018.378
• 论著 • 上一篇
滕兴波1,曹智1,孙海霞1,刘宪金1,杨伟舟1,朱艳2,朱玉广2
TENG Xingbo1, CAO Zhi1, SUN Haixia1, LIU Xianjin1, YANGa Weizhou1, ZHU Yan2, ZHU Yuguang2
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。
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