白藜芦醇对衰老模型小鼠脑组织形态学和氧化应激水平的影响

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目的探讨白藜芦醇对衰老小鼠脑组织的保护作用。方法 54只16周龄雄性昆明小鼠随机分为对照组、衰老组、干预组。对照组皮下注射生理盐水,其余两组皮下注射200 mg/kg BW的D-半乳糖制备衰老小鼠模型,干预组给予22.5 mg/kg BW的白藜芦醇灌胃,其余两组给予0.5%的羧甲基纤维素钠溶液灌胃。干预16周后处死动物,观察小鼠脑组织形态结构,脏器指数,谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、单胺氧化酶(MAO)活性以及丙二醛(MDA)含量的变化。结果与对照组相比,衰老组小鼠神经细胞数量减少且发生变性(P<0.05),脏器指数低于对照组(P<0.05),脑组织GSH-Px、SOD及CAT活性均降低(P<0.05),MAO活性及MDA含量均增高(P<0.05)。与衰老组相比,干预组小鼠神经细胞数量增多(P<0.05),细胞形态明显改善,脏器指数高于衰老组(P<0.05),脑组织GSH-Px、SOD及CAT活性均增高(P<0.05),MAO活性及MDA含量均降低(P<0.05)。结论白藜芦醇能维持衰老小鼠神经细胞正常形态结构,降低其氧化应激水平,对衰老模型小鼠脑组织具有保护作用。 Objective To investigate the protective effect of resveratrol on brain tissue of senile mice. Methods Fifty-four male Kunming mice of 16 weeks old were randomly divided into control group, aging group and intervention group. The control group was subcutaneously injected with saline and the other two groups were injected subcutaneously with 200 mg / kg BW of D-galactose to prepare the aging mouse model. The intervention group was administered with 22.5 mg / kg BW of resveratrol, the other two groups were given 0.5% Sodium carboxymethyl cellulose solution gavage. After 16 weeks of intervention, animals were sacrificed to observe the morphological structure, organ index, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT) Monoamine oxidase (MAO) activity and the content of malondialdehyde (MDA). Results Compared with the control group, the number of neuronal cells in the aging group was decreased and degenerated (P <0.05), the index of organ was lower than that in the control group (P <0.05), the activity of GSH-Px, P <0.05), MAO activity and MDA content increased (P <0.05). Compared with the aging group, the number of neuronal cells in the intervention group increased (P <0.05), the cell morphology was significantly improved, the organ index was higher than the aging group (P <0.05), GSH-Px, SOD and CAT activity were increased (P <0.05), MAO activity and MDA content decreased (P <0.05). Conclusion Resveratrol can maintain the normal morphology and structure of neurons in aging mice and decrease the level of oxidative stress, which may have a protective effect on the brain tissue of aged mice.
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