Naprapathy attenuates neuropathic pain after brachial plexus injury

Abstract

Background: This study was to explore the potential mechanism of naprapathy in treating neuropathic pain (NP) after brachial plexus injury (BPI). Methods: Totally 72 rats were randomly divided into normal group, model control group, and naprapathy group (n=24 per group). A right upper-limb chronic NP model was established, and naprapathy was administered at C5-T1 Jiaji Points on 4th day after modeling. Naprapathy was performed for 15 min once daily with a frequency of 60 per minute. The treatment was applied for altogether 28 days. Cold pain threshold and mechanical pain threshold were measured 1 day before modeling, 3 days after modeling, and 7, 14, 21 and 28 days after naprapathy; 7, 14, 21 and 28 days after naprapathy, rats were killed and the ß-endorphin expression and ?-aminobutyric acid (GABA) content were detected in the thalamus. Results: After 14-day treatment, there was significant difference of mechanical pain threshold between the naprapathy group and the normal group (P<0.05); after treatment for 21 and 28 days, there was no significant difference between the naprapathy group and the normal group (P>0.05); after 28-day naprapathy, there was significant difference of ß-EP expression between the normal group and the naprapathy group (P<0.05), while the difference between model control group and naprapathy group was statistically significant (P<0.05). After 14-day treatment, there was significant difference of GABA content between the model control group and the naprapathy group (P<0.05). After 28-day treatment, significant difference was also found between the model control group and the naprapathy group (P<0.05). Conclusions: After naprapathy, chronic NP is attenuated in rats with BPI, which might be ascribed to the upregulation of ß-endorphin and GABA.