All measurements in this study were done in a criminal fashion: mean values with standard deviations were obtained.Intravitreal injection of LY294002 attenuated the rescue aftereffects of G CSF on RGC in ON crushed eyes, RGC densities in-the central and middle peripheral retina were 10-50 _ 520/mm2 and 560 _ 330/mm2, respectively. These results suggest that the rescue ramifications of G CSF on RGCs were inhibited by intravitreal Bazedoxifene injection of PI3K/AKT inhibitor. The consistent results were shown by the TUNEL assay of RGC layers. The recovery aftereffects of H CSF treated rats had significantly less TUNEL reactive cells in the RGC layers than that in both H CSF and LY294002 treated rats. The outcome demonstrated that anti apoptotic effects of H CSF on RGCs following the ON break function were attenuated by simultaneous intravitreal injection of the PI3K/AKT chemical. Together, these findings suggest that the anti apoptotic effects of H CSF on rat RGCs after ON crush are PI3k/Akt dependent. Double staining studies of p AKT and NeuN within the retinal areas of ON crushed and Gary CSF treated rats at one and fourteen days highlighted that appearance of Metastatic carcinoma p AKT was up regulated in-the RGC sheets and company localized with that of RGCs. In ON crushed retinas and sham operated, G CSF expression was widely distributed within the retinal neurons. The expression of H CSF was increased in the sections of ON crushed and G CSF treated mice. We’ve demonstrated that G CSF administration has neuroprotective results on RGCs after ON crush in a rat model. Our results demonstrate that the anti apoptotic effects of H CSF on RGCs are PI3k/AKT dependent. This was confirmed by the significant decline in RGC survival when intravitreal injection of the chemical was also given. TUNEL assay of RGC levels showed consistent results. The PI3K/AKT ERK, JAK/STAT and route signaling pathways have all been reported order Geneticin for H CSF mediated anti apoptotic results in the CNS damage models. Phosphorylation events occurring in these paths have relief effects on RGCs after an harm. Our western blot analyses confirmed that p AKT signaling in the retinas, like that within the brain swing product was the main signaling event been activated by G CSF administration in rats after ON crush. The IHC studies showed that p AKT was widely up regulated in the retinas of H CSF treated and ON crushed mice. Inhibition of PI3K/AKT indeed interfered with the anti apoptotic action of G CSF, as shown in our RGC morphometry and TUNEL assays. Our double staining of NeuN and p AKT also confirmed that retinal ganglion cells co localize the up rules of p AKT on the ON crushed and Gary CSF addressed retinas.