Abstract
Glaucoma is an advanced nerve disorder described by the deterioration of axon and RGCs. CMCS has been previously used as an anti-apoptotic and anti-oxidant agent. The current study aimed to explore the protective impact of CMCS against H2O2-induced injury in glaucoma in vitro. The relative expression of lncRNA THOR and the protein expression of IGF2BP1 in H2O2-induced RGC-5 cells were detected by RT-PCR and western blot methods respectively. The cell viability was measured using MTT assay while apoptosis rate was measured by flow cytometry. Moreover, ROS level was measured using ROS assay kit. Furthermore, the relations between THOR and IGF2BP1 were determined by using RNA pull-down. The expression of THOR was reduced in H2O2-induced RGCs. Also, RGCs viability was inhibited while the level of ROS and cell apoptosis were enhanced. CMCS treatment considerably enhanced the expression of THOR and IGF2BP1 protein and cell viability but reduced ROS level and cell apoptosis. Moreover, IGF2BP1 protein was positively regulated by lncRNA THOR. CMCS protected the RGCs from oxidative stress via regulating lncRNA THOR/IGF2BP1. CMCS enhanced the cell viability and reduced the cell apoptosis and ROS level and protected RGCs from oxidative stress via lncRNATHOR/IGF2BP1 pathway, potentially suggesting a new therapeutic strategy for the treatment of glaucoma.
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