Vitamin C ascorbic acid (AA) and dehydroascorbic acid (DHA) as an antioxidant have been shown to have protective effects in experimental neurological disorder models such as stroke, ischemia, and epileptic seizures. The present study was conducted to examine the protective effect of AA and DHA on Ka...
Vitamin C ascorbic acid (AA) and dehydroascorbic acid (DHA) as an antioxidant have been shown to have protective effects in experimental neurological disorder models such as stroke, ischemia, and epileptic seizures. The present study was conducted to examine the protective effect of AA and DHA on Kainic acid (KA) neurotoxicity using organotypic hippocampal slice cultures (OHSC). After 12h KA treatment, significant delayed neuronal death was detected in CA3 region, but not in CA1. Intermediate dose of AA and DHA pretreatment significantly prevented cell death and inhibit ROS level, mitochondrial dysfunction and capase-3 activation in CA3 region. In the case of low or high dose, however, AA or DHA pretreatment were not effective. These data suggest that both AA and DHA pretreatment have neuroprotective effects on KA-induced neuronal injury depending on the concentration, by means of inhibition of ROS generation, mitochondrial dysfunction, and caspase-dependent apoptotic pathway.
Vitamin C ascorbic acid (AA) and dehydroascorbic acid (DHA) as an antioxidant have been shown to have protective effects in experimental neurological disorder models such as stroke, ischemia, and epileptic seizures. The present study was conducted to examine the protective effect of AA and DHA on Kainic acid (KA) neurotoxicity using organotypic hippocampal slice cultures (OHSC). After 12h KA treatment, significant delayed neuronal death was detected in CA3 region, but not in CA1. Intermediate dose of AA and DHA pretreatment significantly prevented cell death and inhibit ROS level, mitochondrial dysfunction and capase-3 activation in CA3 region. In the case of low or high dose, however, AA or DHA pretreatment were not effective. These data suggest that both AA and DHA pretreatment have neuroprotective effects on KA-induced neuronal injury depending on the concentration, by means of inhibition of ROS generation, mitochondrial dysfunction, and caspase-dependent apoptotic pathway.
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성능/효과
Representative PI-stained images of increasing dose of AA and DHA (0, 10, 100, 500 and 1000 μM) are shown in Fig. 2A and B. In control cultures, the PI uptake was very low, while in KA only cultures, area of PI-incorporated cell death was broad and deep in CA3 region as compared with the rest of groups (Fig. 2A and B).
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