BCP has been shown to exert a protective role on neurological deficit and neuroinflammation in experimental models, including middle cerebral artery occlusion induced-cerebral ischemia by suppressing the oxidative stress, inflammatory mediators, apoptosis, and reduction in brain edema, as well as preservation of tight junction proteins and repair of blood brain barrier (Zhang et al., 2017; Tian et al., 2019). This evidence concerns the gene OPN1SW and brain ischemia.