This study aimed to investigate the
therapeutic effect of
progesterone on
acute brain injury after
subarachnoid hemorrhage (SAH).
Subarachnoid hemorrhage was induced in male Sprague-Dawley rats (n=72) by endovascular perforation.
Progesterone (8 mg/kg or 16 mg/kg) was administered to rats at 1, 6, and 12h after SAH. Mortality,
neurologic deficits, cell apoptosis, expression of apoptotic markers, the level of
malondialdehyde (MDA) and the activity of
superoxide dismutase (SOD) were assayed at 24h after experimental SAH. Mortality, cell apoptosis and the expression of
caspase-3 were decreased, and improved neurological function was observed in the
progesterone-treated SAH rats. Further, exploration demonstrated that
progesterone significantly reduced the ratio of Bax/Bcl-2 and attenuated the release of
cytochrome c from mitochondria.
Progesterone also induced anti-oxidative effects by elevating the activity of SOD and decreasing MDA content after SAH. Furthermore, dose-response relationships for
progesterone treatment were observed, and high doses of
progesterone enhanced the
neuroprotective effects.
Progesterone treatment could alleviate
acute brain injury after SAH by inhibiting cell apoptosis and decreasing damage due to oxidative stress. The mechanism involved in the anti-apoptotic effect was related to the mitochondrial pathway. These results indicate that
progesterone possesses the potential to be a novel therapeutic agent for the treatment of
acute brain injury after SAH.