参蓉补脑胶囊对老年痴呆模型小鼠学习记忆能力的改善作用及机制研究
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篇名: 参蓉补脑胶囊对老年痴呆模型小鼠学习记忆能力的改善作用及机制研究
TITLE:
摘要: 目的:研究参蓉补脑胶囊对老年痴呆(AD)模型小鼠学习记忆能力的改善作用,并探讨其作用机制。方法:将72只小鼠随机分为空白对照组(生理盐水)、模型组(生理盐水)、吡拉西坦片组(阳性对照,0.80 g/kg)和参蓉补脑胶囊高、中、低剂量组(1.92、0.96、0.48 g/kg),每组12只;除空白对照组小鼠皮下注射等量生理盐水外,其余各组小鼠均每日皮下注射D-半乳糖(150 mg/kg)和腹腔注射亚硝酸钠(50 mg/kg)复制AD小鼠模型;并于造模同时灌胃相应药物,每天1次,连续60 d。末次给药1 h后,设计水迷宫实验测定小鼠逃避潜伏期和90 s内穿越平台位置的次数,苏木精-伊红(HE)染色后观察小鼠大脑皮层病理变化,并采用免疫组织化学法检测小鼠大脑皮层肿瘤坏死因子α(TNF-α)、核转录因子кB p65(NF-кB p65)、磷脂酰肌醇3-激酶(PI3K)和磷酸化蛋白激酶(Akt)蛋白的表达。结果:与空白对照组比较,模型组小鼠逃避潜伏期明显延长(P<0.01),90 s内穿越平台次数显著减少(P<0.01);大脑皮层神经细胞明显损伤,完整神经细胞数显著减少(P<0.01);大脑皮层TNF-α、NF-кB p65、PI3K、Akt蛋白表达水平显著升高(P<0.01)。与模型组比较,除参蓉补脑胶囊低剂量小鼠的逃避潜伏期和大脑皮层TNF-α、NF-кB p65、PI3K、Akt蛋白表达水平差异无统计学意义外(P>0.05),其余各给药组小鼠上述指标均明显改善(P<0.05或P<0.01)。结论:参蓉补脑胶囊能改善AD模型小鼠的学习记忆能力;其机制可能与其抑制小鼠大脑皮层TNF-α、NF-кB p65、PI3K、Akt蛋白的表达,减轻炎症损伤有关。
ABSTRACT: OBJECTIVE: To study the improvement effect of Shenrong bunao capsule on learning and memory ability of Alzheimer’s disease (AD) model mice, and to investigate its mechanism. METHODS: Totally 72 mice were randomly divided into blank control group (normal saline), model group (normal saline), Piracetam tablets group (positive control,0.80 g/kg),Shenrong bunao capsule high-dose,middle-dose and low-dose groups (1.92, 0.96, 0.48 g/kg), with 12 mice in each group. Except that blank control group was given constant volume of normal saline subcutaneously. Other groups were given D-galactose (150 mg/kg) subcutaneously and sodium nitrite (50 mg/kg) intraperitoneally every day to induce AD model. At the same time,they were given relevant medicine intragastrically,once a day, for consecutive 60 d. 1 h after last administration, Morris water maze test was used to measure escape latency and times of crossing the platform within 90 s. HE staining was used to observe pathological changes of cerebral cortex in mice. Immunohistochemistry was used to detect the expressions of TNF-α, NF-κB p65, PI3K and Akt in cerebral cortex of mice. RESULTS: Compared with blank control group, escape latency was prolonged significantly (P<0.01), and the times of crossing the platform within 90 s was decreased significantly in model group (P<0.01). The neurons in cerebral cortex was damaged obviously, and the number of intact neurons was decreased significantly (P<0.01). The protein expressions of TNF-α, NF-κB p65, PI3K and Akt in cerebral cortex were increased significantly (P<0.01). Compared with model group, except that there was no statistical significance in escape latency, protein expressions of TNF-α, NF-кB p65, PI3K and Akt in Shenrong bunao capsule low-dose group (P>0.05), above indexes of other administration groups were improved significantly (P<0.05 or P<0.01). CONCLUSIONS: Shenrong bunao capsule can improve the learning and memory ability of AD model mice, and its mechanism may be related to the inhibiting the protein expressions of TNF-α,NF-κB p65, PI3K and Akt in cerebral cortex region and relieving inflammation injury so as to protect cranial nerve.
期刊: 2019年第30卷第23期
作者: 屈相玲,朴春梅,熊成欢,李平,刘明,周训蓉
AUTHORS: QU Xiangling,PU Chunmei,XIONG Chenghuan,LI Ping,LIU Ming,ZHOU Xunrong
关键字: 参蓉补脑胶囊;老年痴呆模型;核转录因子кB p65;磷脂酰肌醇3-激酶;磷酸化蛋白激酶;肿瘤坏死因子α;小鼠
KEYWORDS: Shenrong bunao capsule; Alzheimer’s disease model; NF-кB p65; PI3K; Akt; TNF-α; Mice
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