Pulsed radiofrequency alleviated neuropathic pain by down-regulating the expression of substance P in chronic constriction injury rat model

BACKGROUND: Pulsed radiofrequency (PRF), as a non-invasive treatment of neuropathic pain (NP), has been widely administered clinically. Previous studies have shown that PRF has the potential to improve hyperalgesia in animal models of NP. However, there have been few reports to clarify whether the mechanism of PRF treatment of NP involves intervention in the expression of substance P (SP). Therefore, this study administered PRF treatment to chronic constriction injury (CCI) model rats and observed the sciatic nerve mechanical pain threshold and SP expression in the spinal cord to explore the mechanism of PRF treatment. METHODS: A total of 96 Sprague-Dawley rats were randomly divided into the sham-surgery-sham-treatment group (S-S group), the sham-surgery-PRF group (S-P group), the CCI-sham-treatment group (C-S group), and the CCI-PRF group (C-P group). The C-S group and the C-P group underwent sciatic nerve CCI, while the other groups received a sham operation. At 14 days after the operation, the C-P group and the S-P group were treated with PRF for 300 s. We recorded the hindpaw withdrawal threshold (HWT) and the thermal withdrawal latency (TWL) of rats in the various groups at baseline, before treatment (0 days), and at 1, 7, 14, and 28 days after treatment. L4 to L6 spinal cord tissues were taken before treatment (0 days) and 1, 7, 14, and 28 days after treatment. The transcription and translation of SP were measured by quantitative polymerase chain reaction and Western blotting, respectively. RESULTS: The HWT and the TWL in the C-P group 28 days after PRF treatment were significantly higher than those in the C-S group (95% confidence interval [CI]: 5.84–19.50, P < 0.01; 95% CI: 2.58–8.69, P = 0.01). The expression of SP in the C-P group 28 days after PRF treatment was significantly lower than that in the C-S group (95% CI: 1.17–2.48, P < 0.01). CONCLUSIONS: PRF may alleviate CCI-induced NP by down-regulating the expression of SP in the spinal cord of CCI model rats.