(+)-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.

GABA:248 μM(EC50)

Aβ诱导的细胞毒性被100μM的(-)和(+)-BORNEOL处理所抑制。冰片处理显著降低了ROS的生成（P < 0.01）。Aβ处理增加了HO-1的表达和Nrf2的核内转移。这种Nrf2的核内转移通过冰片的给药进一步增加。与仅Aβ处理的组相比，(+)-BORNEOL处理的组显著增加了Bcl-2的表达，并降低了Bax的表达[1]。

(+)-borneol（1.0 mg/kg）通过降低诱导型一氧化氮合酶（iNOS）和肿瘤坏死因子-α（TNF-α）的表达，以剂量依赖的方式显著改善梗塞大小和神经评分。值得注意的是，在光栓塞模型的中风中，(+)-borneol展示了对感觉运动功能改善的长期效果，这通过减少树突棘在长度、分支数量和密度上的损失，至少在一定程度上降低了格栅行走任务中的脚失误数量和圆筒任务中的前肢不对称评分。这表明(+)-borneol可以作为缺血性中风的治疗靶标[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].