DL-Borneol

507-70-0

C10H18O

DMSO : >= 100 mg/mL (648.30 mM); H2O : < 0.1 mg/mL (insoluble)

Neuronal Signaling; Membrane Transporter/Ion Channel

DL-Borneol is a racemic mixture of D-Borneol and L-Borneol. DL-Borneol is widely used for the treatment of cardiovascular and cerebrovascular diseases in China. In Vitro: DL-Borneol increases intracellular accumulation of Rho123, and enhances P-gp substrates across the BBB in vitro, and also depresses mdr1a mRNA and P-gp expression. Furthermore, DL-Borneol could activate NF-kappaB and inhibition of NF-kappaB with MG132 and SN50 obscures the P-gp decreases induced by DL-Borneol. 10 ug/mL and 20 ug/mL DL-Borneol significantly increase phosphorylation of IkappaB expression at 30 min after treatment transiently. DL-Borneol treatment decreases P-gp expression in BMECs^[1]. In Vivo: DL-Borneol significantly suppresses the process of epileptogenesis in PTZ-kindled mice. The biochemical alterations induced by PTZ kindling are ameliorated in DL-Borneol-treated animals which is indicated by decreased LPO and increased SOD, GSH, CAT levels. The distinct neuronal damage observed in the kindled group is counteracted by DL-Borneol. Furthermore, it decreases the levels of GFAP which is manifested by reduced immunostaining^[2]. The pathological damages of ischemia-reperfusion have a significant impact on the pharmacokinetic traits of DL-Borneol and that there are some components in Xingnaojing inhibiting the absorption of DL-Borneol^[3].