| 远志寡糖酯改善D-半乳糖致小鼠学习记忆障碍的作用研究 |
| 投稿时间：2024-10-18 修订日期：2024-11-19 点此下载全文
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| 基金项目:国家自然科学基金项目（面上项目，重点项目，重大项目） |
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| 中文摘要:目的：研究远志寡糖酯(Oligosaccharide ester, OE)对D-半乳糖诱导的快速脑老化痴呆小鼠学习记忆能力的改善作用。方法：将8周龄昆明小鼠随机分为对照组、模型组、多奈哌齐组和OE(28.67,57.33 mg/kg)组。通过腹腔注射D-半乳糖诱导脑老化模型,每天灌胃给药1次,持续60 d。通过跳台实验和Morris水迷宫实验检测小鼠的学习记忆功能；收集血清测定SOD活性和MDA含量；采用免疫组织化学染色检测小鼠大脑皮层中BDNF表达水平；采用Western blot法检测小鼠大脑皮层中Akt、CREB及BDNF蛋白表达水平。结果：与空白组比较,模型组逃避潜伏期显著延长(P<0.05),首次穿台潜伏期显著延长(P<0.01),首次跳台潜伏期显著缩短(P<0.01),跳台错误次数显著增加(P<0.01)；SOD活性显著下降(P<0.01),MDA含量显著上升(P<0.01)；p-Akt/Akt、p-CREB/CREB水平及BDNF 表达水平显著降低(P < 0.01)。与模型组比较,OE可以明显缩短小鼠的逃避潜伏期(P<0.05)及首次穿台潜伏期(P<0.01),增加穿台次数(P<0.01),延长首次跳台潜伏期(P<0.05),降低跳台错误次数(P<0.05),改善脑老化小鼠学习记忆的巩固能力和空间辨别能力；增强血清中SOD活性,降低MDA水平(P<0.01)；增加小鼠大脑皮层中p-Akt/Akt(P<0.05)、p-CREB/CREB及BDNF蛋白表达水平(P<0.01),以OE(57.33 mg/kg)组作用更为显著。结论：OE可以改善D-半乳糖诱导的快速脑老化痴呆小鼠的学习记忆障碍,可能与其调控Akt/CREB/BDNF信号通路有关。 |
| 中文关键词:远志寡糖酯 D-半乳糖 学习记忆 抗氧化 Akt/CREB/BDNF信号通路 |
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| Study on the effect of Oligosaccharide esters from Polygala tenuifolia Willd. in ameliorating D-galactose-induced learning memory impairment in mice |
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| Abstract:Objective: To investigate the effect of Oligosaccharide esters from Polygala tenuifolia Willd. (OE) on learning and memory ability in D-galactose induced rapid brain aging dementia mice and its mechanism. Methods:8-week-old Kunming mice were randomly divided into the control group, model group, donepezil group and OE (28.67, 57.33 mg/kg) group, which were administered by gavage once a day for 60 days. Step-down test and Morris water maze test were used to detect the learning and memory ability of mice. SOD activity and MDA content were measured by biochemical kits, the protein expression of BDNF in cerebral cortex of mice was detected by immunohistochemical staining, using Western blot test mice Akt/CREB/BDNF signaling pathways related protein expression. Results: Compared with the control group, the model group had a significantly longer escape latency (P<0.05), a significantly longer latency for the first time through the table (P<0.01), a significantly shorter latency for the first time to jump (P<0.01), and a significantly higher number of jumping errors (P<0.01); a significant decrease in the activity of SOD (P<0.01), and a significant increase in the content of MDA (P<0.01); and significant decreases in the levels of p-Akt/Akt, p-CREB/CREB, and BDNF (P<0.01). Akt, p-CREB/CREB levels and BDNF expression levels were significantly decreased (P<0.01). Compared with the model group, OE could significantly shorten the evasion latency (P<0.05) and the latency of first stage crossing (P<0.01), increase the number of stage crossings (P<0.01), prolong the latency of first stage jumping (P<0.05), and reduce the number of jumping errors (P<0.05), improve the consolidation of learning memories and spatial discrimination ability in the brain-aging mice; enhance the serum SOD activity in serum and reduced MDA level (P<0.01); increased the protein expression levels of p-Akt/Akt (P<0.05), p-CREB/CREB and BDNF in the cerebral cortex of mice (P<0.01), and the effect was more significant in the OE (57.33 mg/kg) group. Conclusion: OE can improve cognitive dysfunction of D-galactose-induced ageing mice, and the mechanism may be related to reduce the oxidative damage of mice, regulating the Akt /CREB/BDNF signaling pathway. |
| keywords:Oligosaccharide esters from Polygala tenuifolia Willd. D-galactose cognitive dysfunction antioxidation Akt/CREB/BDNF signaling pathway |
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