Objective     To investigate the protective effect of apoptosis signal-regulating kinase 1 (ASK1) on high glucoseinduced injury in retinal ganglion cells (RGCs) and its possible mechanism.  Methods     Rat RGCs were isolated

cultured and subjected to high glucose (50 mmol/L) environment to establish an RGCs injury model. Gene silencing of ASK1 was performed by transfection of ASK1 siRNA into RGCs. The mRNA expression of ASK1 was measured by quantitative real-time PCR (qRT-PCR). The protein expression levels of ASK1

total JNK and phosphorylated JNK were detected by Western blotting. Cell growth and viability

and cell proliferation of RGCs were measured by MTT and CCK-8 assays and Ki67 staining

respectively. The apoptosis of RGCs was detected by Annexin-V FITC/PI and TUNEL staining. Caspase-3 activity was measured by fluorescent assay kit.  Results     Cell growth and viability of RGCs was significantly decreased after treated with high glucose for 4 d (P0.05). qRT-PCR measurement showed that ASK1 was significantly up regulated in RGCs treated with high glucose (P0.05). The expression of ASK1 was significantly down regulated in the ASK1 siRNA-transfected RGCs (P0.05)

suggesting a successful silencing of ASK1. The silencing of ASK1 remarkably increased cell growth and viability (P0.05) and proliferation (P0.05)

as well as significantly suppressed the apoptosis (P0.01) and Caspase-3 activity (P0.01). Furthermore

inhibition of ASK1 effectively restricted the phosphorylation of JNK.  Conclusion     ASK1 inhibition has a protective effect on high glucose-induced injury of retinal ganglion cells

which is partly modulated by JNK pathway.