Chaihu Shugan Decoction improves cognitive impairment after epilepsy in rats by regulating hippocampal NMDAR subunits via upregulating ASIC1
10.12122/j.issn.1673-4254.2025.07.17
- VernacularTitle:柴胡疏肝汤通过上调ASIC1蛋白调节NMDAR通道改善大鼠癫痫后的认知障碍
- Author:
Yunhong YU
1
;
Wei XIE
;
Hui LI
Author Information
1. 广东省人民医院//广东省医学科学院//广东省老年医学研究所//南方医科大学,广东 广州 510080
- Publication Type:Journal Article
- Keywords:
epilepsy;
cognitive impairment;
treatment from Gan;
Chaihu Shugan Decoction;
acid sensitive ion channel;
NMDAR
- From:
Journal of Southern Medical University
2025;45(7):1506-1512
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the therapeutic mechanism of Chaihu Shugan(CHSG)Decoction for improving cognitive impairment in rats with epilepsy induced by lithium chloride and pilocarpine.Methods Male SD rat models of cognitive impairment model after epilepsy induced by intraperitoneal injection with lithium chloride and pilocarpine were randomly divided into 5 groups(n=12)for treatment with daily gavage of saline,donepezil(90 mg/kg),or CHSG Decoction at 2.5,5.0,10,20 and 40 g/kg for 4 consecutive weeks,with 10 rats with intraperitoneal injection with saline as the blank control group.Morris water maze test was used to evaluate cognitive and behavioral changes of the rats after treatment.The mRNA and protein expressions of ASIC1,NR1,NR2A and NR2B in the hippocampus of rats were detected using RT-qPCR and Western blotting.Results Compared with those with saline treatment,the rat models treated with CHSG Decoction at 5 and 10 g/kg showed significantly shortened escape latency and prolonged stay in the target quadrant with increased number of platform crossings in Morris water maze test.CHSG Decoction treatment at the two doses significantly increased ASIC1,NR1,NR2A and NR2B protein expressions in the hippocampus of the rat models,and their mRNA expression levels were all increased significantly after the treatment at the doses above 2.5 g/kg.Conclusion CHSG Decoction can improve cognitive impairment in rats after epilepsy possibly by regulating the expression and channel activity of NMDAR protein and its subunit protein via upregulating ASIC1 to modulate neuronal excitability and synaptic plasticity in the hippocampus.
