The outcome suggest upregulation of Bax protein levels in ischemiasensitive retinal neurons situated in the inner part of the retina following transient ischemia. Immunocytochemical staining of normal retinas shown that the Hh pathway inhibitors protein was barely noticeable in most layers of the retina by the present approach. The failure to detect the bax gene product in the tissues might connect with the lesser volume of Bax protein being expressed in the normal retina than the sensitivity of our method can detect, as the mRNA of bax was expressed in the control retina. The current study was based upon analysis of paraffin sections. Actually, in cryostat sections using various anti peptide antisera for Bax developed by Krajewski et al., Isenmann et al. Noted immunoreactivity in the retinal ganglion cells w16x. Transient forebrain ischemia has been demonstrated to require apoptotic cell death in the CA1 area of the hippocampus, which supposedly occurred as early as 12 h after 10 min ischemia and reached a at 48 h in the span of reperfusion w33x. The depth of Bax expression in the CA1 neurons of hippocampus was reported to improve as time passes and peaked at 6 h after 10 min global cerebral ischemia w21x. But, contrary to these early involvement of the apoptotic process in the span of reperfusion, there are some observations that 5 min forebrain ischemia did not induce apoptosis until 48 h after Lymphatic system ischemic impact w25x. Also, it was reported after 5 min forebrain ischemia that upregulation of Bax peaked at 72 h in gerbil hippocampus w12x with future maximum occurrence of DNA fragmentation at 96 h. In retinal ischemia, the number of ganglion cells was not reduced 1?4 days after 45 min ischemia, then it reduced substantially 7 days after ischemia under our experimental settings w1x. Apoptotic cells described by the TUNEL labeled cells peaked at 24 h after ischemia. The comparatively early appearance of apoptotic cells in the course of reperfusion after retinal ischemia was also suggested by Bu?chi who noticed morphological changes of apoptosis happening in the GCL and INL particularly at 1 day and 3 h after 60 min pressure caused ischemia Crizotinib molecular weight w4x. When it comes to temporal profile of gene expression concerning apoptosis, the current study demonstrated that bax mRNA expression increased with time and peaked at 24 h after ischemia. Hence, in retinal ischemia, the process appears to be motivated to work early in the length of reperfusion. Optic nerve axotomy has been proven to result in delayed neuronal death through the procedure of apoptosis of retinal ganglion cells in adult mice, rabbits, and monkeys w3.