(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate

Sprague-Dawley (male, 280-300 g, middle cerebral artery occlusion/reperfusion model)^[1]

1 mg/kg; 3 mg/kg; 5 mg/kg

p.o.; administered 0.5 h before MCAO, 1 h after MCAO, and 1 h after reperfusion

Significantly reduced MCAO/R-induced cerebral infarct volume, edema volume, and neurological deficit scores, and significantly increased rotarod duration compared to vehicle-treated rats.
Produced dose-dependent effects, with the 5 mg/kg dose causing the greatest reduction in infarct volume (p < 0.01 vs vehicle) and edema volume (p < 0.01 vs vehicle), and the largest improvement in rotarod duration (p < 0.01 vs vehicle).
Significantly prevented MCAO/R-induced depletion of glutathione (GSH) levels in ipsilateral brain tissue.
Significantly alleviated MCAO/R-induced increases in thiobarbituric acid reactive substances (TBARS) levels in ipsilateral brain tissue at 3 mg/kg and 5 mg/kg doses.
Significantly increased the Bcl-2/Bax expression ratio in ipsilateral brain tissue compared to vehicle-treated rats.
Significantly inhibited the MCAO/R-induced increase in the cleaved caspase-3/procaspase-3 expression ratio at 3 mg/kg and 5 mg/kg doses.
Significantly inhibited the MCAO/R-induced increase in the p-p38/p38 expression ratio, and significantly reduced the upregulation of inducible nitric oxide synthase (i-NOS) and cyclooxygenase-2 (COX-2) expression in ipsilateral brain tissue.
Significantly upregulated MCAO/R-reduced phosphatidylinositol 3-kinase (PI3K) expression, and significantly alleviated the MCAO/R-induced decreases in the p-Akt/Akt and p-CREB/CREB expression ratios in ipsilateral brain tissue.