An experimental research on the analgesic effect and underlying mechanism of BTX-A for rat knee osteoarthritis
10.3969/j.issn.1001-1242.2017.06.008
- VernacularTitle:A型肉毒毒素对膝骨性关节炎大鼠模型镇痛效果及机制的实验研究
- Author:
Wenjun MA
;
Ying LIANG
- Keywords:
botulinum toxin type A;
knee osteoarthritis;
Nav1.8 sodium channel;
paw withdrawal latency;
analgesia
- From:
Chinese Journal of Rehabilitation Medicine
2017;32(6):649-653
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluate the analgesic effect of botulinum toxin type A (BTX-A) in osteoarthritis model and the changes of Nav1.8 protein expression in spinal ganglia changes.Method:Animal model of knee osteoarthritis (KOA) was established by intra-articular injection of 4％ papain solution 0.3ml into SD rat right knee.After the formation of arthritis,they were randomly divided into two groups at the 2nd day:BTX-A group (n=10):intra-articular injection of 5μl BTX-A 0.1IU;WFI group (n=10):intra-articular injection of 5μl water.No papain or BXT-A was given to the sham group (n=10).At the 1st,3rd,5th day after injection,we tested the pain behavior,thermal pain threshold,and sodium channel 1.8 (Nav1.8) protein expression in spinal ganglion by using immunohistochemistry.Result:Analysis of spontaneous pain behavior showed abnormal gait caused by rat osteoarthritis.Comparing with the WFI group,abnormal gait caused by osteoarthritis improved significantly in BTX-A group.At day 5 it improved more significantly than day 1 and day 3.Thermal pain threshold of BTX-A group increased more than that of WFI group (P＜0.05) at any time point.Abnormal high Nav1.8 protein in model rats decreased in spinal ganglia for BTX-A group.Conclusion:The intra-articular injection of BTX-A may play the analgesic effect in the model of KOA by down-regulating of the expression of Nav1.8 protein in spinal ganglia and reduction in the central sensitization to pain stimulation.
