The studies of 1 week following fore mind ischemia were just like that of Fig. G, H.. Negative staining was observed in CAl parts of all of the parts examined for the Bcl 2 immunohistochemistry, kinase chemical selection for screening even though positive immunotaining was recognized in choroid plexus as an internal positive control.. The serial sections used for the particular in situ nick end labeling technique for DNA breaks in the previous study were considered again, and the direct comparison between the expression of Bax and Bcl 2 proteins and the DNA fragmentation in the CAl region was done.. The increase of the immunoreactivity of Bax started at 48 h subsequent forebrain ischemia and the time of the immunostaining depth was 72 h. To the contrary, the DNA fragmentation started to be seen at 72 h following forebrain ischemia and the time of the DNA fragmentation was 96 h. The expression of Afatinib price Bcl 2 protein was not recognized whenever you want after the transient forebrain ischemia. It’s known that adult brain often shows no immunohistochemically detectable expression of Bcl 2 protein.. Shimazaki et al. Noted that 2 min of ischemia avoided the delayed neuronal death and induced tolerance to subsequent ischemia, and that in this condition, enhanced expression of Bcl 2 protein was observed in the CAl location of the gerbil hippocampus. It is suggested that, in our present study, more severe ischemia which induced total delayed neuronal death in the CAl location prevented the increase of Bcl 2 protein. Recent studies have described the postischemic DNA fragmentation in the hippocampus of experimental ischemic models as a key phenomenon for the delayed neuronal death, However, apoptotic figures, often recognized in common apototic cells, have Metastatic carcinoma been never noticed in the hippocampal CAl neurons following transient forebrain ischemia. Furthermore, the ultrastructural study of the morphological changes in the hippocampal CAl neurons following transient forebrain ischemia suggested that the delayed neuronal death is different from regular apoptosis, Therefore, it remains questionable perhaps the delayed neuronal death is apoptosis or necrosis. In today’s research, the increase of the immunoreactivity of apoptosis inducing protein, Bax was shown in the CAl location following transient forebrain ischemia. Moreover, the peak of the immunostaining intensity of Bax after the Ivacaftor 873054-44-5 ischemic insult preceded the peak appearance of the DNA fragmentation in the CAl location of the hippocampus. This finding suggests that overexpression of Bax may play a significant part to cause the DNA fragmentation in the CAl neurons. Our results provide a new evidence which shows that apoptotic process is associated with the pathophysiology of the delayed neuronal death, while the detailed connection between the function of Bax protein and the delayed neuronal death continues to be unclear.