The role of AMPK/mTOR signal pathway in brain injury following chronic intermittent hypoxia in growing rats

OBJECTIVE: To investigate the role of AMPK-mTOR signal pathway in brain injury induced by chronic intermittent hypoxia (CIH) in young rats.

MATERIALS AND METHODS: Forty healthy male Sprague-Dawley rats (3-4 weeks old, weighing 80-100 g) were randomly assigned to four groups: 2-week-CIH group (2IH), 4-week-CIH group (4IH), 2-week-simulated air control group (2AC) and 4-week-simulated air control group (4AC). TUNEL staining was used to detect the cell apoptosis in the hippocampus and pre-frontal cortexes, respectively. The Western blot was conducted to analysis the P-AMPK (Phospho-AMP-activated protein kinase) and P-mTOR (phosphorylated mammalian target of rapamycin) protein expression.

RESULTS: The neurons apoptosis in the hippocampus and pre-frontal cortex in 2IH and 4IH groups increased significantly, compared with that of in 2AC and 4AC groups, (p<0.05, respectively). Moreover, 4IH group exhibited significantly increased apoptosis rates than 2IH group (p<0.05). 2IH and 4IH groups exhibited increased protein expression levels of P-AMPK in the hippocampus and prefrontal cortexes compared with 2AC and 4AC groups (p<0.05, respectively), whereas the protein expression of P-mTOR decreased after CIH treatment (p<0.05, respectively). Higher expression levels of P-AMPK and lower levels of P-mTOR were observed in 4IH group compared to 2IH group. No difference of apoptotic cells and protein expression of P-AMPK and P-mTOR was exhibited between 2AC and 4AC groups.

CONCLUSIONS: CIH induces neural apoptosis in a time-dependent manner by activating AMPK and inhibiting mTOR phosphorylation in young rats.

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