AIM: To study the mechanisms of how hyperbaric oxygen treatment (HBOT) reduced neuronal apoptosis following forebrain ischemia reperfusion. METHODS: Changes of the expression of protein Bcl-2 or Bax were observed in CA1 region of gerbil hippocampus following HBOT on ischemia reperfusion 3 days using the method of labelled streptavidin biotin (LSAB) immunohistochemistry staining. For this purpose gerbils were exposed to the 0.15 MPa and 0.25 MPa HBO 60 min every day for 3 successive days. RESULTS: The expression of protein Bcl-2 in hippocampus CA1 was significantly increased in HBOT groups (P < 0.01), and changes in 0.25 MPa groups were greater than those in 0.15 MPa groups (P < 0.01). The expression of protein Bax in hippocampus CA1 was not changed significantly in HBOT groups. CONCLUSION: HBO can induce the expression of Bcl-2, which is the mechanism of neuronal protecting effect of HBOT.
AIM: To study the mechanisms of how hyperbaric oxygen treatment (HBOT) reduced neuronal apoptosis following forebrain ischemia reperfusion. METHODS: Changes of the expression of protein Bcl-2 or Bax were observed in CA1 region of gerbil hippocampus following HBOT on ischemia reperfusion 3 days using the method of labelled streptavidin biotin (LSAB) immunohistochemistry staining. For this purpose gerbils were exposed to the 0.15 MPa and 0.25 MPa HBO 60 min every day for 3 successive days. RESULTS: The expression of protein Bcl-2 in hippocampus CA1 was significantly increased in HBOT groups (P < 0.01), and changes in 0.25 MPa groups were greater than those in 0.15 MPa groups (P < 0.01). The expression of protein Bax in hippocampus CA1 was not changed significantly in HBOT groups. CONCLUSION:HBO can induce the expression of Bcl-2, which is the mechanism of neuronal protecting effect of HBOT.