Rapid nontranscriptional activation of endothelial nitric oxide synthase mediates increased cerebral blood flow and stroke protection by corticosteroids
J. Clin. Invest. Florian P. Limbourg, et al. 110:1729 doi:10.1172/JCI15481 [Go to this article.]

Figure 3
Activation of PI3K/Akt mediates neuroprotection. (a) Neuroprotection by dexamethasone is mediated by GR and PI3K. Cerebral infarct volume after MCAo in response to dexamethasone (20 mg/kg), RU486 (200 mg/kg) and LY294002 (5 mg/kg, n = 7–11). Vehicle and dexamethasone groups are identical to those in figure 1a. *P < 0.05 vs. vehicle, **P < 0.05 vs. dexamethasone. RU, RU486; LY, LY294002. (b) In vivo activation of PI3K by dexamethasone. PI3K activity from mouse brain tissue immunoprecipitated with GR or p85 antibody. The product of the kinase reaction, PIP₃, was visualized by autoradiography. (c) The left panel shows Akt activity and total Akt from mouse brain tissue. Mice were treated with vehicle or dexamethasone, with or without actinomycin D (ActD) (5 mg/kg), RU486, or LY294002. The right panel shows P-Akt (S473) and total Akt from mouse aortae. P, phosphorylation form of the protein. Representative experiments are shown.