红景天苷对东莨菪碱诱导阿尔茨海默病模型大鼠炎症因子的影响

Influence of salidroside on inflammatory factors of model rats with Alzheimer's disease induced by scopolamine

  • 摘要:
      目的  探讨红景天苷对东莨菪碱诱导阿尔茨海默病模型大鼠炎症因子的影响。
      方法  将40只雄性SD大鼠随机分为空白组、模型组以及红景天苷高、中、低剂量组。采用腹腔注射东莨菪碱的方法建立阿尔茨海默病模型大鼠,其中空白组和模型组给予生理盐水10 mL/(kg·d), 高、中、低剂量组分别给予75、50、25 mg/(kg·d)红景天苷(需将纯度>95%红景天苷粉末与双蒸水混合),连续给药21 d。比较各组大鼠行为学实验、病理实验和ELISA实验结果。
      结果  Morris水迷宫实验显示,实验第2天,高剂量组行动轨迹与空白组相似,大鼠对平台位置的记忆能力优于模型组; 高剂量组大鼠目标平台象限搜索时间与穿越平台次数比均高于模型组,模型组大鼠潜伏期时间长于中剂量组,差异均有统计学意义(P < 0.05)。HE染色显示高剂量组与空白组细胞形态大致相似,神经细胞普遍较细,细胞排列较规则; 模型组海马神经元明显受损,细胞散在。与空白组相比,模型组大鼠脑肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)水平升高,差异有统计学意义(P < 0.05); 与模型组相比,高剂量组和中剂量组大鼠脑TNF-α、IL-1β水平降低,差异有统计学意义(P < 0.05)。
      结论  红景天苷能显著增强AD大鼠的学习记忆能力,减轻海马神经元的损伤,调节中枢炎症状态,修复海马神经元的病理损伤,其机制可能与改善炎症反应、增强免疫功能有关。

     

    Abstract:
      Objective  To investigate the influence of salidroside on inflammatory factors of model rats with Alzheimer′s disease induced by scopolamine.
      Methods  A total of 40 male SD rats were randomly divided into blank group, model group and high-, medium- and low-dose salidroside groups. Model rats with Alzheimer′s disease were established by intraperitoneal injection of scopolamine. The blank group and model group were given normal saline with the dose of 10 mL/(kg·d), and the high, medium and low dose groups were given 75, 50 and 25 mg/(kg·d) salidroside (salidroside powder with purity >95% should be mixed with double distilled water) for 21 days. The results of behavioral experiment, pathological experiment and ELISA experiment were compared.
      Results  Morris water maze test showed that on the second day of the experiment, the action track of the high-dose group was similar to that of the blank group, and the memory ability of the rats to the platform position was better than that of the model group; the ratio of target platform quadrant search time and times of crossing platform in the high-dose group were significantly higher than those in the model group, and the latency time in the model group was significantly longer than that in the medium-dose group (P < 0.05). HE staining showed that the cell morphology of the high-dose group was roughly similar to that of the blank group, and the nerve cells were generally thin and arranged regularly; hippocampal neurons in the model group were significantly damaged and scattered. Compared with the blank group, the brain tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the model group were significantly higher (P < 0.05); compared with the model group, brain TNFα and IL-1β levels in high-dose group and medium-dose group were significantly lower (P < 0.05).
      Conclusion  Salidroside can significantly enhance the learning and memory abilities of AD rats, reduce the damage of hippocampal neurons, regulate the central inflammatory state, and repair the pathological damage of hippocampal neurons, and its mechanism may be related to improvement of inflammatory response and enhancement of immune function.

     

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