In vitro, Borneol enhances the intracellular accumulation of Rho123 and facilitates the transport of P-gp substrates across the blood-brain barrier (BBB). Additionally, it downregulates the expression of mdr1a mRNA and P-gp. Borneol activates NF-κB, and the inhibition of NF-κB with MG132 and SN50 attenuates the reduction in P-gp induced by Borneol. Treatment with 10 μg/mL and 20 μg/mL Borneol transiently increases the phosphorylation of IκB expression at 30 min post-treatment. Furthermore, Borneol treatment leads to a decrease in P-gp expression in brain microvascular endothelial cells (BMECs)[1].

Borneol significantly counteracts the process of epileptogenesis in PTZ-kindled mice. Borneol-treated animals show amelioration of biochemical alterations induced by PTZ kindling, as evidenced by decreased lipid peroxidation (LPO) and increased levels of superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT). The distinct neuronal damage observed in the kindled group is suppressed by Borneol. Additionally, Borneol reduces the levels of GFAP, as indicated by reduced immunostaining[3]. The pharmacokinetic traits of Borneol are significantly affected by the pathological damages of ischemia-reperfusion, and there are components in Xingnaojing that inhibit the absorption of Borneol[2].