Study on analgesic effect and mechanism of sophoridine oxide on neuropathic pain model mice
10.12092/j.issn.1009-2501.2025.09.002
- VernacularTitle:氧化槐定碱对神经病理性疼痛模型小鼠的镇痛作用及机制研究
- Author:
Fan CHENG
1
;
Lei SHI
;
Xiujuan ZHANG
;
Yanli HU
;
Jinxian GAO
Author Information
1. 甘肃省人民医院药剂科,兰州 730000,甘肃;甘肃中医药大学药学院,兰州 730000,甘肃
- Publication Type:Journal Article
- Keywords:
oxysophoridine;
neuropathic pain;
gamma aminobutyric acid;
brain;
spinal dorsal horn
- From:
Chinese Journal of Clinical Pharmacology and Therapeutics
2025;30(9):1165-1173
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To study the mechanism of oxy-sophoridine(OSR)in relieving neuropathic pain(NP).METHODS:The analgesic effect of OSR was observed by measuring mechanical pain sensitivity.By combining OSR with agonists and antagonists re-lated to synthesis and metabolism of gamma ami-nobutyric acid(GABA),the mechanism related to analgesic effects of OSR and GABA nervous system is studied.The expression of c-Fos immunopositive cells and the expression of c-Fos and Glutamic acid decarboxylase(Glutamic acid decarboxylase 67)in brain and spinal cord were detected by immunoflu-orescence staining.Co-expression of GAD67,GABA transporter 1(gamma-Aminobutyric acid Transport-er 1,GAT-1)immunopositive cells.RESULTS:Com-pared with Sham group,spared nerve injury(SNI)group showed increased mechanical pain sensitivi-ty,increased expression of c-Fos immunopositive cells,decreased and increased co-expression of c-Fos and GAD67 and GAT-1 immunopositive cells,re-spectively.Compared with SNI group,mechanical algesia in OSR 500 and 1 000 mg/kg groups was de-creased,algesia in OSR 250 mg/kg combined with antagonist group was decreased,and algesia in OSR 500 mg/kg combined with agonist group was increased.The co-expression of c-Fos and GAD67 immunopositive cells in the brain and spinal cord of OSR 500 mg/kg group increased,while the co-ex-pression of c-Fos and GAT-1 decreased.CONCLU-SION:OSR has a good analgesic effect on NP mice induced by SNI.The mechanism is that OSR increas-es the content of central GABA by up-regulating GABAergic neurons in brain and spinal cord.
