Wang Qingge, Zhao Xiaohui, He Yuxuan, Liu Feixiang, Zhang Yunke
Talent Pool of Henan Province Hospital of Traditional Chinese Medicine, Zhengzhou 450000, China.
First Clinical Medical College of Henan University of Chinese Medicine, Zhengzhou 450000, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2025 Aug 20;45(8):1589-1598. doi: 10.12122/j.issn.1673-4254.2025.08.03.
To exple the mechanism of Granules (QXZG) for enhancing synaptic plasticity in aging rats.
Forty SD rats were randomized into control group, aging model group, donepezil treatment group, and QXZG treatment group (=10). Except for the control rats, all the rats were subjected to daily intraperitoneal injection of D-galactose for 8 consecutive weeks to induce brain aging, and donepezil hydrochloride and QXZG suspension were administered by gavage during modeling. After the interventions, the rats were evaluated for general conditions, behavioral changes, oxidative stress indicators, hippocampal pathologies, and expressions of the brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) pathway, p16, and synaptic plasticity-associated proteins.
The rats in the model group exhibited obvious aging phenotypes such as yellowing of the teeth and hair, body weight loss, and impaired learning and memory abilities, with decreased serum SOD and GSH-Px activities and increased serum MDA level. The rat models also showed obvious pathological changes, reduced Nissl bodies, and elevated p16 protein expression in the hippocampal CA1 region, with significantly decreased expression levels of BDNF, TrkB, CREB and synaptic plasticity proteins SYN, GAP43, and PSD95. Treatment with QXZG alleviated the aging phenotypes in the rat models, improved their learning and memory abilities and pathological changes in the hippocampal CA1 region, reduced oxidative stress and p16 protein expression, and promoted the expressions of the BDNF/TrkB pathway proteins and synaptic plasticity proteins.
QXZG enhances synaptic plasticity and reduces oxidative stress in aging rats possibly by upregulating the BDNF/TrkB signaling pathway proteins, thereby delaying brain aging and improving learning and memory abilities of the rats.
探讨芪参益智颗粒(QXZG)增强衰老大鼠突触可塑性的机制。
将40只SD大鼠随机分为对照组、衰老模型组、多奈哌齐治疗组和QXZG治疗组(每组10只)。除对照组大鼠外,其余大鼠连续8周每日腹腔注射D-半乳糖诱导脑衰老,建模期间分别灌胃给予盐酸多奈哌齐和QXZG混悬液。干预后,对大鼠的一般状况、行为变化、氧化应激指标、海马病理学以及脑源性神经营养因子(BDNF)/酪氨酸激酶受体B(TrkB)通路、p16和突触可塑性相关蛋白的表达进行评估。
模型组大鼠出现明显的衰老表型,如牙齿和毛发变黄、体重减轻、学习记忆能力受损,血清超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性降低,血清丙二醛(MDA)水平升高。大鼠模型还表现出明显的病理变化,海马CA1区尼氏体减少,p16蛋白表达升高,BDNF、TrkB、环磷腺苷反应元件结合蛋白(CREB)以及突触可塑性蛋白突触素(SYN)、生长相关蛋白43(GAP43)和突触后致密物95(PSD95)的表达水平显著降低。QXZG治疗可减轻大鼠模型的衰老表型,改善其学习记忆能力和海马CA1区的病理变化,降低氧化应激和p16蛋白表达,促进BDNF/TrkB通路蛋白和突触可塑性蛋白的表达。
QXZG可能通过上调BDNF/TrkB信号通路蛋白增强衰老大鼠的突触可塑性并降低氧化应激,从而延缓脑衰老,改善大鼠的学习记忆能力。