Protective limb remote ischemic post-conditioning against high-intraocular-pressure-induced retinal injury in mice

作     者：Qi-Jiang Zhu Lei Zhang Shuang-Yu Lyu Zhan-Jun Cui En-She Jiang Jun Wang 

作者机构：School of Clinical MedicineHenan UniversityKaifeng 475001Henan ProvinceChina Henan International Joint Laboratory for Nuclear Protein RegulationHenan UniversityKaifeng 475001Henan ProvinceChina School of Basic Medical SciencesHenan UniversityKaifeng 475001Henan ProvinceChina Institute of Nursing and HealthSchool of Nursing and HealthHenan UniversityKaifeng 475001Henan ProvinceChina 

出 版 物：《International Journal of Ophthalmology(English edition)》 (国际眼科杂志（英文版）)

年 卷 期：2022年第15卷第4期

页      面：560-567页

核心收录：

学科分类：1002[医学-临床医学] 100212[医学-眼科学] 10[医学] 

基　　金：Supported by the National Natural Science Foundation of China(No.31300884 No.81803573) 

主　　题：retina ischemic conditioning high intraocular pressure 

摘      要：AIM: To determine whether limb remote ischemic postconditioning(LRIC) protects against high-intraocularpressure(IOP)-induced retinal injur y, and to identify underlying molecular mechanisms. METHODS: In mice, IOP was increased to 110 mm Hg for 50 min and LRIC applied to the unilateral leg for three occlusion cycles(5 min/release). Three animal groups(control, high IOP, and high IOP+LRIC) were arranged in this study. Plasma was collected from LRIC treated mice. Retinal histology, oxidative stress were determined by histological section staining and chemical kit. C/EBP homologous protein(CHOP), and Iba-1 parameters were evaluated by immunofluorescent staining and Western blot. RESULTS: The data showed that LRIC treatment alleviated the retinal histological disorganization and ganglion cell loss induced by high IOP. The CHOP, Iba-1 expression and oxidative stress marker also were inhibited by LRIC treatment. To further explore underlying mechanisms, plasma from LRIC treated animals was intravenously transfused into high-IOP animals. The results showed plasma injection decreased caspase 9 expression and DHE staining signals compared with that in high IOP retinas. CONCLUSION: These data suggest that LRIC treatments exert retinal protective effects against high-IOP *** humoral factors release into the circulation by LRIC may contribute to homeostatic protection by reducing monocyte infiltration and/or microglia activation.