论文部分内容阅读
目的观察淫羊藿苷(Ica)对Aβ_(25-35)致阿尔采末病(AD)大鼠的空间学习记忆能力障碍的改善作用及可能机制。方法 SD大鼠43只,随机分为对照组(n=13)、模型组(n=15)及Ica(120 mg·kg~(-1))组(n=15),每日灌胃给药1周后,右侧海马内注射Aβ_(25-35)10μg制备AD模型,制模后继续给药3周。Morris水迷宫检测大鼠空间学习记忆能力,ELISA检测大鼠海马肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)蛋白的含量,Western blot检测半胱氨酸天冬氨酸蛋白酶(caspase-3)蛋白的表达,real time RT-PCR检测海马TNF-α,IL-6和caspase-3 mRNA的表达。结果水迷宫结果表明,与对照组比较,模型组大鼠平均逃避潜伏期明显延长,进入平台次数、原平台象限滞留时间百分比及原平台象限运动距离百分比均显著降低(P<0.05);与模型组比较,Ica组大鼠的平均逃避潜伏期明显缩短,进入平台次数、原平台象限滞留时间百分比及原平台象限运动距离百分比均明显增加(P<0.05)。模型组大鼠海马中的TNF-α和IL-6含量及caspase-3蛋白表达明显高于对照组(P<0.05);Ica组大鼠海马中的TNF-α和IL-6含量及caspase-3蛋白表达均显著降低(P<0.05),TNF-α,IL-6及caspase-3的mRNA表达也显著低于模型组(P<0.05)。结论 Ica可能通过抑制炎症因子TNF-α,IL-6以及凋亡基因caspase-3的表达改善Aβ_(25-35)诱导的AD大鼠空间学习记忆能力。
Objective To observe the effect of icariin (Ica) on the spatial learning and memory impairment caused by Aβ_ (25-35) -induced Alzheimer’s disease (AD) in rats and its possible mechanism. Methods Forty-three SD rats were randomly divided into control group (n = 13), model group (n = 15) and Ica (120 mg · kg -1) groups (n = 15) One week after treatment, 10 μg of Aβ_ (25-35) was injected into right hippocampus to prepare AD model. Morris water maze was used to detect spatial learning and memory in rats. ELISA was used to detect the content of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) in hippocampus of rats. Western blot was used to detect cysteine aspartate The expression of caspase-3 protein was detected by real time RT-PCR. The expression of TNF-α, IL-6 and caspase-3 mRNA in the hippocampus were detected by real time RT-PCR. Results The water maze results showed that compared with the control group, the mean escape latency of the model group was significantly prolonged. The number of platforms entering the platform, the percentage of the original platform quadrant retention time and the percentage of the original platform quadrant movement distance were significantly decreased (P <0.05) In comparison, the mean escape latency of rats in Ica group was significantly shortened. The number of times of entering the platform, the percentage of the original platform quadrant retention time and the percentage of the original platform quadrant movement distance were significantly increased (P <0.05). The content of TNF-α, IL-6 and the expression of caspase-3 in the hippocampus of the model group were significantly higher than those in the control group (P <0.05). The content of TNF-α and IL- 3 protein (P <0.05), and the mRNA expressions of TNF-α, IL-6 and caspase-3 were significantly lower in model group than those in model group (P <0.05). Conclusions Ica may improve Aβ 25-35-induced spatial learning and memory in AD rats by inhibiting the expression of inflammatory cytokines TNF-α and IL-6 and caspase-3.