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

Abstract

To determine whether limb remote ischemic post-conditioning (LRIC) protects against high-intraocular-pressure (IOP)-induced retinal injury, and to identify underlying molecular mechanisms. In mice, IOP was increased to 110 mm Hg for 50min and LRIC applied to the unilateral leg for three occlusion cycles (5min/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. 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. These data suggest that LRIC treatments exert retinal protective effects against high-IOP injury. Endogenous humoral factors release into the circulation by LRIC may contribute to homeostatic protection by reducing monocyte infiltration and/or microglia activation.