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机构地区:[1]暨南大学药学院药理教研室,广东广州510632
出 处:《中成药》2006年第10期1466-1469,共4页Chinese Traditional Patent Medicine
摘 要:目的:研究小檗碱(Berberine)对D-半乳糖诱导的糖基化模型大鼠并发脑损害的干预作用。方法:D-半乳糖(150mg/kg.d,ip)连续给药8周,诱导糖基化模型大鼠,并于第3周开始给予小檗碱高(300 mg/kg)、中(150 mg/kg)、低(75mg/kg)剂量处理6周。测定红细胞醛糖还原酶活性、糖化血红蛋白、血清果糖胺和晚期糖基化终末产物(advanced glyca-tion end-products,AGEs)含量及脑组织中AGEs含量、脑神经细胞内钙离子水平,并以透射电镜观察脑内海马神经原线粒体的变化。结果:小檗碱高、中剂量明显降低模型组大鼠红细胞醛糖还原酶活性,抑制糖化产物的形成(P<0.01),降低脑组织中AGEs及脑神经细胞内钙的含量(P<0.05,P<0.01),保护海马神经原线粒体结构的完整性。结论:小檗碱具有抑制D-半乳糖诱导的蛋白糖基化反应,并对糖基化状态并发的脑神经细胞损害具有保护作用。AIM: To observe the improvement effects of berberine on glycated brain damages in model rats induced by D-galactose. METHODS: The model rats of protein glycation were induced by intraperitoneal administration of D-galactose (150 mg/kg·d) for 8 weeks,and all rats were treated with berberine (high dose 300 mg/ kg, middle dose 150 mg/kg, low dose 75 mg/kg) for 6 weeks. The activity of aldose reductase in red blood cells, the amount of glycated products ( fructosamine in serum, glycohaemoglobin, advanced gtycation end-products), and the content of AGEs in brain tissue, calcium ion in brain cells were measured. Moreover, mitochondria in brain hippocampus cells were observed under electronic microscope. RESULTS: High dose and middle dose of berberine could decrease the activity of aldose reductase in red blood cells (P〈0.01 ) ,and inhibit the formation of glycation products significantly in model rats induced by D-galactose (P〈0.01 ). Also,berberine could decrease the content of AGEs in brain and the level of calcium ions in brain cells ( P〈0.05, P〈0.01 ), and also decrease lesions deglycated brain damages through inhibiting the glycation reaction in rats induced by D-galactose.
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