[The change and mechanism of apoptosis in the hippocampal CA1 region of rats exposed to intermittent hypoxia].

OBJECTIVE: To investigate the effect of intermittent hypoxia on rat hippocampal oxidative stress and neuron apoptosis in the hippocampal CA1 region. METHODS: Thirty six healthy male Wistar rats were randomly divided into three groups of 12 each: a control (NC) group, an intermittent hypoxia (IH) group and a sustained hypoxia (SH) group. The levels of Malondialdehyde (MDA) and Superoxide dismutase (SOD) were detected by colorimetric method. Western blotting was used to examine the expression of p-JNK and p-c-jun. TUNEL was used to detect the neuron apoptosis in the hippocampal CA1 region. RESULTS: The level of MDA (nmol/mg protein) in the hippocampal CA1 region in IH group (1.61 +/- 0.39) was significantly higher than those in NC group (1.25 +/- 0.29) and in SH group (1.34 +/- 0.24), F = 4.185, P < 0.05; the level of SOD (NU/mg protein) in IH group (45 +/- 13) was significantly lower than those in NC group (58 +/- 12) and in SH group (56 +/- 10), F = 4.338, P < 0.05. There were no significant differences between SH and NC groups in the level of MDA or in the activity of SOD (P all > 0.05). The expression of p-JNK and p-c-jun in IH group were 2.1 and 2.3 times the expression in the NC group respectively. The apoptotic indices of IH group (0.30 +/- 0.16) was significantly elevated as compared with group NC (0.12 +/- 0.07) and SH (0.17 +/- 0.09), F = 7.766, P < 0.01. CONCLUSION: Oxidative stress associated with IH in the hippocampal CA1 region can activate JNK signaling pathway, leading to the apoptosis of hippocampal neuron. This maybe the pathophysiological basis of obstructive sleep apnea hypopnea syndrome with neurobehavioral impairments.