Neuroprotective and Antioxidant Effects of the Butanol Fraction Prepared from Opuntia ficus-indica var. saboten

Abstract

− The fruits and stems of Opuntia ficus-indica var. saboten have been reported to exhibit a variety of pharmacological actions, including antioxidant, analgesic, anti-inflammatory, and anti-ulcer effects. In the present study, we evaluated effects of the butanol fraction (SK OFB901) prepared from the 50% ethanol extract of the stems on various types of neuronal injuries induced by oxidative stress, excitotoxins, and amyloid β (A β ) in primary cultured rat cortical cells. Its antioxidant and radical scavenging activities were also evaluated by cell-free bioassays. We found that SK OFB901 strongly inhibited the oxidative neuronal damage induced by H 2 O 2 or xanthine/xanthine oxidase. In addition, it exhibited marked inhibition of the excitotoxic neuronal damage induced by glutamate, N-methyl-D-aspartic acid, or kainate. Furthermore, the A β(25-35) -induced neurotoxicity was also significantly attenuated by SK OFB901. It was found to inhibit lipid peroxidation initiated by Fe 2+ and L-ascorbic acid in rat brain homogenates and scavenge 1,1-diphenyl-2-picrylhydrazyl free radicals. These results indicate that the butanol fraction prepared from the stems of Opuntia ficus-indica var. saboten exerts potent antioxidant and neuroprotective effects through multiple mechanisms, implying its potential applications for the prevention or management of neurodegenerative disorders associated with oxidative stress, excitotoxicity, and A β .

An overview and update on the chemical composition and potential health benefits of Opuntia ficus‐indica (L.) Miller

“…saboten ) stems n‐butanol fraction prepared from 50% ethanol extract exhibited marked neuroprotective effects in primary cultured rat cortical cells, as it strongly inhibited the H 2 O 2 or xanthine/xanthine oxidase induced oxidative damage and glutamate, N ‐methyl‐ d ‐aspartic acid, or kainate induced excitotoxic neuronal damage. In addition, it also significantly inhibited the A β(25–35) ‐induced neurotoxicity (Cho et al, 2007). Other neuroprotection mechanisms for the stem n‐butanol fraction and also its hydrolysis product were reported by Lee et al (2006).…”