Effect of gastrodin on chemotherapy-induced neuropathic pain and its mechanism: an analysis via CX3CR1 pathway
10.3760/cma.j.issn.1671-8925.2015.07.010
- VernacularTitle:从CX3CR1通路探讨天麻素对化疗痛的作用机制
- Author:
Ni LUO
1
;
Denghui GONG
;
Weihong ZHENG
;
Jun ZHENG
;
Jinzhi ZHANG
;
Ju WAN
;
Yuxing LI
Author Information
1. 三峡大学医学院国家中药药理三级实验室
- Keywords:
Vincristine;
Chemotherapy-induced neuropathic pain;
Microglial
- From:
Chinese Journal of Neuromedicine
2015;14(7):695-699
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the inhibited effect of gastrodin on chemotherapy-induced neuropathic pain and its mechanism.Methods Fifty SD rats,chosen according to the threshold of pain,were randomly divided into 5 groups(n=10):control group,model group,and gastrodin treatment groups (30 mg/kg,60 mg/kg and 120 mg/kg).Vincristine (125 μg/kg,i.p.) was administered on alternate days to establish chemotherapy-induced neuropathic pain models in the model group and gastrodin treatment groups,and then,on the 9th d of modeling rats in the gastrodin treatment groups were treated with different doses of gastrodin,while those in the control group and model group were given normal saline on the 16th d of modeling.Paw withdrawal mechanical threshold and thermal pain threshold were measured;protein expressions of CX3CR1 and p-p38MAPK were detected by Western blotting,and tumor necrosis factor α (TNF-α) protein expression was detected by ELISA.Results As compared with control group,model group had significantly decreased pain threshold and increased protein expressions of CX3CR1,p-p38MAPK and TNF-α (P＜0.05);as compared with those in the model group,the pain threshold increased and the expressions of CX3CR1,p-p38MAPK and TNF-α decreased in 60 mg/kg and 120 mg/kg gastrodin treatment groups,with significant differences (P＜0.05).Conclusion Gastrodin can relieve the chemotherapy-induced neuropathic pain,probably by inhibiting the expressions of CX3CR1 and p-p38MAPK in the activation passageway of microglial cells in the spinal cord,and then,reducing the expression of TNF-α.
