Effects of Perilla Seed Pomace Extract on Aging-Induced Cognitive Dysfunction in SAMP8 Mice
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Perilla seed pomace and its constituent phytochemicals have anti-inflammatory, antioxidant, and anti-aging benefits. However, its effects on aging-related cognitive decline are not well-studied. Therefore, the antioxidant and neuroprotective properties of perilla seed pomace extract (PSE) on hydrogen peroxide (H2O2)-induced neuronal cell death were examined. Additionally, the efficacy of PSE in ameliorating age-related cognitive impairment was evaluated in vivo using the senescenceaccelerated mouse prone 8 (SAMP8). PSE showed free radical scavenging activities and inhibited FeSO4-H2O2-induced lipid peroxidation. In HT22 neuronal cells, PSE protected against H2O2-induced oxidative stress and cytotoxicity by restoring mitochondrial membrane potential and attenuating excessive reactive oxygen species production. Furthermore, PSE reversed the H2O2-inducedupregulation of apoptotic markers (Bax, cleaved caspase-3) and downregulation of the anti-apoptotic marker Bcl2. Additionally, the protein levels of antioxidant enzymes (Catalase, SOD, and GPx) were increased under conditions of H2O2-induced oxidative stress. In vivo, PSE significantly ameliorated cognitive deficits, as evidenced by improved performance in passive avoidance and Morris water maze test results. Further, PSE reduced the accumulation of lipid peroxides and significantly increased catalase and glutathione peroxidase activity in the brain. These findings suggest that PSE attenuates agingrelated cognitive deficits by enhancing antioxidant defenses in the brain, highlighting its potential as a dietary intervention for aging-related cognitive decline.
Abstract
Perilla seed pomace and its constituent phytochemicals have anti-inflammatory, antioxidant, and anti-aging benefits. However, its effects on aging-related cognitive decline are not well-studied. Therefore, the antioxidant and neuroprotective properties of perilla seed pomace extract (PSE) on hydrogen peroxide (H2O2)-induced neuronal cell death were examined. Additionally, the efficacy of PSE in ameliorating age-related cognitive impairment was evaluated in vivo using the senescenceaccelerated mouse prone 8 (SAMP8). PSE showed free radical scavenging activities and inhibited FeSO4-H2O2-induced lipid peroxidation. In HT22 neuronal cells, PSE protected against H2O2-induced oxidative stress and cytotoxicity by restoring mitochondrial membrane potential and attenuating excessive reactive oxygen species production. Furthermore, PSE reversed the H2O2-inducedupregulation of apoptotic markers (Bax, cleaved caspase-3) and downregulation of the anti-apoptotic marker Bcl2. Additionally, the protein levels of antioxidant enzymes (Catalase, SOD, and GPx) were increased under conditions of H2O2-induced oxidative stress. In vivo, PSE significantly ameliorated cognitive deficits, as evidenced by improved performance in passive avoidance and Morris water maze test results. Further, PSE reduced the accumulation of lipid peroxides and significantly increased catalase and glutathione peroxidase activity in the brain. These findings suggest that PSE attenuates agingrelated cognitive deficits by enhancing antioxidant defenses in the brain, highlighting its potential as a dietary intervention for aging-related cognitive decline.