Qixiong Zuogui Granules enhance synaptic plasticity in aging rats by regulating the BDNF/TrkB signaling pathway.
10.12122/j.issn.1673-4254.2025.08.03
- Author:
Qingge WANG
1
;
Xiaohui ZHAO
2
;
Yuxuan HE
2
;
Feixiang LIU
3
;
Yunke ZHANG
3
Author Information
1. Talent Pool of Henan Province Hospital of Traditional Chinese Medicine, Zhengzhou 450000, China.
2. First Clinical Medical College of Henan University of Chinese Medicine, Zhengzhou 450000, China.
3. Department of Encephalopathy, First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, China.
- Publication Type:Journal Article
- Keywords:
BDNF/TrkB signaling pathway;
Qixiong Zuogui Granules;
brain aging;
learning and memory;
synaptic plasticity
- MeSH:
Animals;
Brain-Derived Neurotrophic Factor/metabolism*;
Neuronal Plasticity/drug effects*;
Signal Transduction/drug effects*;
Rats, Sprague-Dawley;
Receptor, trkB/metabolism*;
Rats;
Aging;
Drugs, Chinese Herbal/pharmacology*;
Male;
Oxidative Stress;
Hippocampus/metabolism*
- From:
Journal of Southern Medical University
2025;45(8):1589-1598
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To exple the mechanism of Qixiong Zuogui Granules (QXZG) for enhancing synaptic plasticity in aging rats.
METHODS:Forty SD rats were randomized into control group, aging model group, donepezil treatment group, and QXZG treatment group (n=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.
RESULTS: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.
CONCLUSIONS: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.
