All dimensions in this study were performed in a criminal fashion: indicate values with standard deviations were obtained.Intravitreal injection of LY294002 attenuated the rescue effects of H CSF on RGC in ON crushed eyes, RGC densities in-the central and mid peripheral retina were 10-50 _ 520/mm2 and 560 _ 330/mm2, respectively. These results suggest the rescue aftereffects of G CSF on RGCs were inhibited by intravitreal Gefitinib clinical trial injection of PI3K/AKT inhibitor. The consistent results were shown by the TUNEL assay of RGC layers. The rescue effects of H CSF treated rats had significantly less TUNEL reactive cells in the RGC layers than that in LY294002 treated rats and both H CSF. The outcome demonstrated that anti apoptotic effects of G CSF on RGCs after the ON break event were attenuated by multiple intravitreal injection of the inhibitor. Together, these findings suggest that the anti apoptotic effects of G CSF on rat RGCs after ON break are PI3k/Akt dependent. Double staining reports of p AKT and NeuN in the parts of ON crushed and G CSF treated rats at one and fourteen days created that appearance of Lymph node p AKT was up regulated in the RGC layers and company local with that of RGCs. In ON crushed retinas and sham operated, G CSF term was widely distributed in the retinal neurons. The appearance of G CSF was improved within the sections of ON crushed and H CSF treated rats. We have demonstrated that G CSF government has neuroprotective effects on RGCs after ON break in a rat model. Our results show that the anti apoptotic effects of H CSF on RGCs are PI3k/AKT dependent. This was demonstrated by the significant decrease in RGC survival when intravitreal injection of the PI3k/AKT chemical was also given. TUNEL analysis of RGC levels showed consistent results. The PI3K/AKT path, JAK/STAT and ERK signaling pathways have all been reported supplier Bicalutamide for G CSF mediated anti apoptotic results in the CNS damage models. Phosphorylation events occurring in these pathways have relief results on RGCs after an injury. Our western blot analyses confirmed that p AKT signaling within the retinas, like that in the head stroke product was the primary signaling event been activated by G CSF administration in mice after ON crush. The IHC studies showed that p AKT was widely up regulated within the retinas of H CSF treated and ON crushed rats. Inhibition of PI3K/AKT indeed interfered with the anti apoptotic action of H CSF, as shown in our RGC morphometry and TUNEL assays. Our double staining of p AKT and NeuN also proved that retinal ganglion cells co localize the up restrictions of p AKT on the ON crushed and H CSF treated retinas.