Int J Biol Sci 2016; 12(8):1032-1040. doi:10.7150/ijbs.15624
Rapamycin Reduced Ischemic Brain Damage in Diabetic Animals Is Associated with Suppressions of mTOR and ERK1/2 Signaling
1. Department of Endocrinology, General Hospital of Ningxia Medical University, Yinchuan 750004, China
The objectives of the present study are to investigate the activation of mTOR and ERK1/2 signaling after cerebral ischemia in diabetic rats and to examine the neuroprotective effects of rapamycin. Ten minutes transient global cerebral ischemia was induced in straptozotocin-induced diabetic hyperglycemic rats and non-diabetic, euglycemic rats. Brain samples were harvested after 16 h of reperfusion. Rapamycin or vehicle was injected 1 month prior to the induction of ischemia. The results showed that diabetes increased ischemic neuronal cell death and associated with elevations of p-P70S6K and Ras/ERK1/2 and suppression of p-AMPKα. Rapamycin ameliorated diabetes-enhanced ischemic brain damage and suppressed phosphorylation of P70S6K and ERK1/2. It is concluded that diabetes activates mTOR and ERK1/2 signaling pathways in rats subjected to transient cerebral ischemia and inhibition of mTOR by rapamycin reduces ischemic brain damage and suppresses the mTOR and ERK1/2 signaling in diabetic settings.
Keywords: Cerebral ischemia, Diabetes, ERK1/2, mTOR, Rapamycin
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How to cite this article:
Liu P, Yang X, Hei C, Meli Y, Niu J, Sun T, Li PA. Rapamycin Reduced Ischemic Brain Damage in Diabetic Animals Is Associated with Suppressions of mTOR and ERK1/2 Signaling. Int J Biol Sci 2016; 12(8):1032-1040. doi:10.7150/ijbs.15624. Available from http://www.ijbs.com/v12p1032.htm