Polysaccharides of Momordica charantia have been reported to be the primary bioactive components that confer its antioxidant activity. To some degree, antioxidants may provide beneficial effects on neuronal damage ind...Polysaccharides of Momordica charantia have been reported to be the primary bioactive components that confer its antioxidant activity. To some degree, antioxidants may provide beneficial effects on neuronal damage induced by seizures. However, the protective effects of Momordica charantia polysaccharides (MCPs) on seizures remain unclear. In this study, our purpose was to investigate the effects of MCPs on oxidative stress and neurodegeneration in an experimental Kainic acid (KA)-induced rat seizure model. MCPs treatments decreased the level of malondialdehyde (MDA) and increased the activities of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus of the KA-induced animal model. Moreover, MCPs significantly attenuated KA-induced neuronal loss in the CA1 and CA3 hippocampal regions. Based on these results, MCPs exert neuroprotective effects by attenuating KA-induced neuronal damage in the brain through their free radical scavenging activities.展开更多
文摘Polysaccharides of Momordica charantia have been reported to be the primary bioactive components that confer its antioxidant activity. To some degree, antioxidants may provide beneficial effects on neuronal damage induced by seizures. However, the protective effects of Momordica charantia polysaccharides (MCPs) on seizures remain unclear. In this study, our purpose was to investigate the effects of MCPs on oxidative stress and neurodegeneration in an experimental Kainic acid (KA)-induced rat seizure model. MCPs treatments decreased the level of malondialdehyde (MDA) and increased the activities of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus of the KA-induced animal model. Moreover, MCPs significantly attenuated KA-induced neuronal loss in the CA1 and CA3 hippocampal regions. Based on these results, MCPs exert neuroprotective effects by attenuating KA-induced neuronal damage in the brain through their free radical scavenging activities.
