In the central nervous system, Asiaticoside has been shown to attenuatein vitro neuronal damage caused by exposure toβ-amyloid.In vivo studies demonstrated that Asiaticoside could attenu-ate neurobehavioral, neurochemical and histological changes in transient focal middle cerebral artery occlusion animals. In addition, Asiaticoside showed anxiolytic effects in acute and chronic stress animals. However, its potential neuroprotective properties in glutamate-induced excito-toxicity have not been fully studied. We investigated the neuroprotective effects of Asiaticoside in primary cultured mouse cortical neurons exposed to glutamate-induced excitotoxicity invoked by N-methyl-D-aspartate. Pretreatment with Asiaticoside decreased neuronal cell loss in a con-centration-dependent manner and restored changes in expression of apoptotic-related proteins Bcl-2 and Bax. Asiaticoside pretreatment also attenuated the upregulation of NR2B expression, a subunit of N-methyl-D-aspartate receptors, but did not affect expression of NR2A subunits. Additionally, in cultured neurons, Asiaticoside significantly inhibited Ca2+ influx induced by N-methyl-D-aspartate. These experimental ifndings provide preliminary evidence that during excitotoxicity induced by N-methyl-D-aspartate exposure in cultured cortical neurons, the neu-roprotective effects of Asiaticoside are mediated through inhibition of calcium inlfux. Aside from its anti-oxidant activity, down-regulation of NR2B-containing N-methyl-D-aspartate receptors may be one of the underlying mechanisms in Asiaticoside neuroprotection.

Objective: To investigate the effect of anthopleurin-Q (AP-Q) on the intracellular Ca2+ concentration ([Ca2+ ]i) in cultured cortical astrocytes of rats. Methods: The [Ca2+ ]i was monitored by calcium imaging with Ca2+ sensitive fluorescent probe fura-2. Results: A concentration of 300 nmol/L AP-Q increased the [Ca2+ ]i in astrocytes by (136.98%±35.63%) (n=28),when compared with the baseline level. Furthermore, the elevation of [Ca2+]i was prevented by extracellular calcium free solution or when the extracellular Na+ was replaced by NMDG+ , and was decreased by Ni+ ,a non-specific antagonist of Na+/Ca2+ exchanger. Conclusion: AP-Q induced the intracellular [Ca2+ ]i elevation in cultured rat cortical astrocytes via activating the reverse mode of Na+/Ca2+ exchanger. AP-Q may be a useful tool to develop experimental model of seizures.