Study on the mechanism of Jiawei xiaochaihu decoction inhibiting hippocampal neuronal apoptosis in epileptic mice via regulating AKT/Bcl-xL/Bax/Caspase-3 signaling axis
- VernacularTitle:加味小柴胡汤调控AKT/Bcl-xL/Bax/Caspase-3信号轴抑制癫痫小鼠海马神经元凋亡的机制研究
- Author:
Ling LU
1
;
Sheng ZHUANG
2
;
Yijue QIN
1
;
Haishun QU
1
;
Yanwei YANG
1
;
Weicheng XU
1
Author Information
1. Dept.of Traditional Chinese Medicine，People’s Hospital of Guangxi Zhuang Autonomous Region，Nanning 530021，China
2. Dept. of Joint Surgery，The Second People’s Hospital of Nanning，Nanning 530031，China
- Publication Type:Journal Article
- Keywords:
Jiawei xiaochaihu decoction;
epilepsy;
AKT/Bcl-xL/Bax/Caspase-3 signaling axis;
neuronal apoptosis
- From:
China Pharmacy
2026;37(13):1728-1734
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To explore the mechanism of Jiawei xiaochaihu decoction against hippocampal neuronal apoptosis in acute epileptic model mice. METHODS Thirty-six male KM mice were randomly divided into four groups with 9 mice in each group： normal control group （normal saline）， epilepsy model group （normal saline）， Jiawei xiaochaihu decoction group [7 g/（kg·d）] and carbamazepine group [positive control， 30 mg/（kg·d）]. Except for the normal control group， the acute epilepsy model was established in the other groups. After successful modeling， mice in each group were given corresponding drugs or normal saline by intragastric administration once a day for 2 consecutive weeks. After drug intervention， the ultrastructure and pathological morphology of hippocampal CA1 region were observed. The number of TUNEL-positive cells in hippocampus was detected， and the expression levels of protein kinase B （AKT）， Caspase-3， B-cell lymphoma-extra large （Bcl-xL）， Bcl-2-associated X protein （Bax）， as well as the ratio of phosphorylated AKT（p-AKT） to AKT were determined. RESULTS Compared with the normal control group， severe ultrastructural and pathological damages were observed in the hippocampal CA1 region of epilepsy model group； the number of TUNEL-positive cells was significantly increased （ P ＜0.05）. The expression levels of p-AKT and Bcl-xL were significantly down-regulated （ P ＜0.05）， while the Bax and Caspase-3 were significantly up-regulated （ P ＜0.05），accompanied by a remarkable decrease of p-AKT/AKT ratio （ P ＜0.05）. Compared with the epilepsy model group， hippocampal tissue ultrastructure， pathological damage， and the aforementioned indicators were significantly improved in Jiawei xiaochaihu decoction group （ P ＜0.05）. CONCLUSIONS Jiawei xiaochaihu decoction can inhibit hippocampal neuronal apoptosis in acute epileptic mice， and its mechanism may be related to activating AKT phosphorylation， increasing p-AKT/AKT ratio， up-regulating Bcl-xL expression and down-regulating the expression of Bax and Caspase-3.
