(+)-BORNEOL (d-Borneol) is a natural bicyclic monoterpene used for analgesia and anesthesia in traditional Chinese medicine; enhances GABA receptor activity with an EC50 of 248 μM.

Aβ-induced cell cytotoxicity was inhibited by 100 μM of (-) and (+) borneol treatment. Treatment of borneol significantly decreased ROS generation (P < 0.01). The expression of HO-1 and nuclear translocation of Nrf2 were increased by Aβ treatment. This nuclear translocation of Nrf2 was further increased by administration of borneol. Compared with the Aβ treated group, the (+) borneol treated group significantly increased Bcl-2 expression with decreased expression of Bax[1].

(+)-borneol (1.0 mg/kg) significantly ameliorated infarct size and neurological scoresvia reducing the expression of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-α) in a dose dependent manner. Notably, (+)-borneol showed long-term effects on the improvement of sensorimotor functions in the photothrombotic model of stroke, which decreased the number of foot faults in the grid-walking task and forelimb asymmetry scores in the cylinder task, at least in part through reducing loss of dendritic spines in the length, brunch number and density. Suggest that (+)-borneol could serve as a therapeutic target for ischemic stroke[2].

Oxidative stress was induced by administering 50 μM Aβ into SH-SY5Y cells. Neuroprotective effect of commercially available borneol was examined by determining cell viability with the MTT assay. Intracellular reactive oxygen species (ROS) generation was measured using a fluorometer with further examination of heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) expression. Apoptosis was examined by measuring the ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax)[1].

To mimic a typical human stroke, which does not undergo reperfusion, used a permanent MCAO in this study. For investigating the role of (+)-borneol in permanent cerebral ischemia, 45 male Sprague-Dawley rats were randomly divided into the sham group, the vehicle-treated group and the (+)-borneol-treated groups (1.0 mg/kg), with 15 rats in each group. The terminal half-life (t1/2) of borneol was 2 h following cerebral ischemia-reperfusion. We subjected the rats to pMCAO and administered drugs by tail intravenous injection 2 hours and 5 hours after pMCAO, respectively. The sham group and the vehicle-treated group were injected with vehicle administration. Neurologic scores were assessed at 48 hours after reperfusion[2].