Zheng Y, Wang XL, Mo FF, Li M.
Low-dose dexamethasone has been widely used for the prevention of nausea
and vomiting after chemotherapy and surgical procedures and to treat
motion sickness due to its minimal adverse effects, but the mechanisms
underlying its anti-motion sickness effects are poorly understood.
Previous studies have demonstrated that the endocannabinoid system is
suppressed by motion sickness but stimulated by dexamethasone. The aim
of the present study was to determine whether dexamethasone has an
anti-motion sickness effect in rats and to elucidate the mechanism of
this action. We used HPLC-MS/MS to measure the plasma concentrations of
anandamide and 2-arachidonoylglycerol+1-arachidonoylglycerol, and we
employed real-time quantitative PCR (qRT-PCR) and/or Western blot
analysis to assay the expression of N-acylphosphatidyl-ethanolamine
hydrolyzing phospholipase D, sn-1-selective diacylglycerol lipase, fatty
acid hydrolase, monoacylglycerol lipase and endocannabinoid CB1
receptor in the dorsal vagal complex and stomach of rats exposed to a
motion sickness protocol. The results showed that dexamethasone lowered
the motion sickness index and restored the levels of endogenous
cannabinoids and the expression of the endocannabinoid CB1 receptor,
which declined after the induction of motion sickness, in the dorsal
vagal complex and stomach.