厚朴对小鼠脑老化损伤的保护作用及其可能机制

Protective effect and possible mechanism of Magnolia officinalis on brain aging damage in mice

目的探讨厚朴对小鼠脑老化损伤的保护作用及其可能机制。方法60只SPF级雄性昆明小鼠随机分成对照组、模型组、低剂量组、中剂量组和高剂量组。Morris水迷宫实验评估各组小鼠的学习记忆能力。超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-Px)试剂盒评估各组小鼠氧化应激水平。TUNEL染色评估神经细胞凋亡的情况。结果与对照组相比,模型组小鼠的逃避潜伏期、脑组织MDA含量和神经细胞凋亡率均明显升高,在平台象限的停留时间和穿越次数均明显降低,脑组织SOD和GSH-Px含量均明显降低(P<0.05)。低剂量、中剂量和高剂量的厚朴处理后,脑老化小鼠的逃避潜伏期、脑组织MDA含量和神经细胞凋亡率均明显降低,在平台象限的停留时间和穿越次数均明显升高,脑组织SOD和GSH-Px含量均明显升高(P<0.05)。结论厚朴可显著改善脑老化引起的认知功能障碍,其机制可能与降低氧化损伤和神经细胞凋亡有关。

Objective To investigate the protective effect and mechanism of Magnolia officinalis on brain aging injury in mice.Methods Sixty male Kunming mice were randomly divided into control group,model group,low dose group,medium dose group and high dose group.Morris water maze test was used to evaluate the learning and memory ability.Superoxide dismutase(SOD),malondialdehyde(MDA)and glutathione peroxidase(GSH-Px)kits were used to evaluate the oxidative stress level.TUNEL staining was used to evaluate the neuronal apoptosis.Results Compared with the control group,the escape latency,the content of MDA and the rate of neuronal apoptosis in the model group were significantly increased(P<0.05).The residence time and crossing times of the model group were significantly decreased(P<0.05).The levels of SOD and GSH-Px in the brain tissue of the model group were decreased(P<0.05).After low-dose,medium-dose and high-dose Magnolia officinalis treatment,the escape latency,the MDA content and neuronal apoptosis rate of brain aging mice were significantly reduced(P<0.05).The residence time and crossing times of the model group were significantly increased(P<0.05).The levels of SOD and GSH-Px in the brain tissue of mice in the model group were increased(P<0.05).Conclusion Magnolia officinalis can significantly improve cognitive impairment in brain aging mice,and its mechanism may be related to the reduction of oxidative damage and neuronal apoptosis..