the results of this study show that the progressive loss of RGC over the course of weeks and the decrease in inner retinal thickness are a direct response to the prolonged duration of implementing 45 mmHg IOP to the rat eye.Our studies show that increasing the duration of 45 mmHg IOP to 5 7 h was sufficient to enzalutamide produce irreversible damage to ON axons and RGCs, without injuring the outer levels of the retina. The reduction in axons and RGC density correlated with the duration of hypertension, as indicated from the ONDS, GCL cell density, retinal layer thickness, and DTMR described RGC density studies. According to these results, we further picked a 7 h period of hypertension as our standard research protocol because it caused the most damage in just a practical time frame for an experimental procedure. The pressure caused RGC damage wasn’t instantly apparent after the insult, losing of RGC as assessed by DTMR labeled cells within the retina became more severe since the article method time extended, such that approximately 50-ish of RGCs vanished 28 days later. The extended application of moderate physical form and external structure ocular hypertension allows analysis of the dynamics of preliminary morphological, molecular, and functional changes under controlled conditions, which supplies insight in to the effects of moderate short-term elevated IOP on RGCs and the possible underlying mechanisms of RGC injury throughout the early stages of glaucoma. Several components could possibly be responsible for RGC injury induced by elevated IOP. Apoptosis was noticed in the GCL subsequent IOP elevation. The effect demonstrated by this method was likely the result of apoptosis in RGCs. Currently time, it is not clear where the first primary injury site is. The excessive stress may damage the RGC soma PFT alpha directly, but it can also initiate damage by compressing the RGC axons, which may hinder intra axonal transport of pro success compounds, such as for instance trophic factors. Alternately, pressure induced retention of the retinal arteries can cause mild ischemia in certain retinal areas. Like, the inner retina, which includes a high metabolic demand and the blood circulation of which comes by the central retinal artery, might be more susceptible to metabolic stress induced by the insult in comparison with the outer retina. There is a well known need to develop glaucoma therapies that target mechanisms apart from IOP get a handle on. Defending the retina from glaucoma damage can be as crucial as controlling IOP. Like, JNK inhibitors such as SP600125 have already been shown to reduce neuronal cell death in the brain along with the retina. Such inhibitors force away rat hippocampal CA1 cell loss brought on by transient mind ischemia/reperfusion. SP600125 also safeguards against excitotoxicity induced apoptosis of RGCs. In our study, we discovered that SP600125 substantially preserved RGC density in rats compared to the car treated group after 7 h of IOP elevation. The outcomes of this study suggest that SP600125 disrupts the JNK cascade of events responsible for RGC apoptosis and supports RGC survival.