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β-Amyloid Protein 유도 기억손상 및 신경세포독성에 대한 미강유의 억제효과
Inhibitory Effect of Rice Bran Oil on β-Amyloid Protein (25-35)-Induced Memory Impairment and Neurotoxicity
Background : Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive memory loss, cognitive impairment and personality defects accompanied by diffuse structural abnormalities in the brain. The major pathological hallmarks of AD include beta amyloid (Aß) protein deposition, presence of neurofibrillary tangles and neurodegeneration of cholinergic neurons. Aß, a 39-43 amino acid proteolytic fragment of amyloid precursor protein, is the major constituent of the senile plaques. Rice bran, the major byproduct of the rice milling industry, is the source of a high quality vegetable oil. Rice bran oil (RBO) has attracted much medicinal attention for its strong hypocholesterolemic properties because of its balanced fatty acid composition and high levels of antioxidant phytochemicals such as oryzanols, tocopherols and tocotrienols. The present study aims to investigate the protective effect of RBO against Aß (25-35)-induced neurotoxicity in in vitro and in vivo. Methods and Results : Memory impairment was produced by intracerebroventricular (i.c.v) microinjection of 15 nmol Aß (25-35) and measured by passive avoidance test in ICR mice. Glutathione concentration, lipid peroxidation rate and acetylcholine esterase activity were measured in mice brain. The expression levels of phosphorylated mitogen activated proteins kinases (MAPKs), inflammatory factors, and anti-apoptotic and pro-apoptotic proteins in mice brains were detected by Western blot. Cerebral cortical neuronal cells were cultured from 15-days-old fetus. Cortical neurons were incubated with 10 μM Aß (25-35) for 36 h. Cell viability was measured by MTT assay. Chronic treatments of RBO (0.1-1 ml/kg, 8 days, p.o.) protected against memory impairment induced by Aß (25-35). Depletion of glutathione level, lipid peroxidation and increased acetylcholine esterase activity by the treatment with Aß (25-35) were inhibited by administration of RBO. The increase of phosphorylated MAPKs, inflammatory factors, and proapoptotic proteins and the decrease of antiapoptotic protein in Aß (25-35)-administered mice brain were significantly inhibited by treatment with RBO. RBO (0.1-5ul/ml) inhibited 10μM Aß (25-35)-induced neuronal cell death in cultured cortical neurons. Conclusion : The present study suggests the role of RBO as a promising therapeutic for neurodegenerative diseases like AD and stroke.
