Opuntia ficus-indica attenuates neuronal injury in in vitro and in vivo models of cerebral ischemia.

Abstract We examined whether the methanol extract of Opuntia ficus-indica (MEOF) has a neuroprotective action against N -methyl- d -aspartate (NMDA)-, kainate (KA)-, and oxygen–glucose deprivation (OGD)-induced neuronal injury in cultured mouse cortical cells. We also evaluated the protective effect of MEOF in the hippocampal CA1 region against neuronal damage evoked by global ischemia in gerbils. Treatment of neuronal cultures with MEOF (30, 300, and 1000 μg/ml) inhibited NMDA (25 μM)-, KA (30 μM)-, and OGD (50 min)-induced neurotoxicity dose-dependently. The butanol fraction of Opuntia ficus-indica (300 μg/ml) significantly reduced NMDA (20 μM)-induced delayed neurotoxicity by 27%. Gerbils were treated with MEOF every 24 h for 3 days (0.1, 1.0, and 4.0 g/kg, p.o.) or for 4 weeks (0.1 and 1.0 g/kg, p.o.), and ischemic injury was induced after the last dose. Neuronal cell damage in the hippocampal CA1 region was evaluated quantitatively at 5 days after the ischemic injury. When gerbils were given doses of 4.0 g/kg (3 days) and 1.0 g/kg (4 weeks), the neuronal damage in the hippocampal region was reduced by 32 and 36%, respectively. These results suggest that the preventive administration of Opuntia ficus-indica extracts may be helpful in alleviating the excitotoxic neuronal damage induced by global ischemia.