Hyperbaric Oxygen Mediated PI3K/Akt/mTOR Pathway in Inhibiting Delayed Cerebral Vasospasm after Subarachnoid Hemorrhage

Delayed cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) is a serious complication. This article aimed to explore the mechanism of hyperbaric oxygenation (HBO) inhibiting delayed CVS after SAH. The 60 SD rats were grouped: normal control group (NC), sham operation group (Sham), SAH Model (Model), and HBO treatment group. The SAH model was established by injecting blood twice into the cisterna magna (CM), and the neurological function of the rats were evaluated by modified Garcia scale. The plasma of the rats was collected at 1, 3, 6, and 9 days after HBO treatment. Plasma levels of PI3K/Akt/mTOR pathway-related proteins were detected by Western blot (WB). TUNEL method was used to observe the apoptosis rate of basilar artery (BA) endothelial cells (ECs). Hematoxylin-eosin staining (HE) staining was used to observe the inner diameter and the thickness of vessel wall of rat cerebral arteries. The relationship between mTOR and middle cerebral artery spasm was analyzed. As against the Model, the neurological function was visibly increased, the expressions of Bcl-2, PI3K, mTOR, and p-Akt/Akt protein in plasma were visibly increased, the expression of Bax protein was visibly decreased, and the degree of CVS was visibly reduced in the HBO group (all P < 0.05). The level of mTOR is negatively correlated with the degree of CVS after SAH, and HBO can inhibit the occurrence of delayed CVS.