Gua Sha attenuates thermal hyperalgesia and decreases proinflammatory cytokine expression in serum in rats with lumbar disc herniation induced by autologous nucleus pulposus.

OBJECTIVE

To investigate the analgesic effect of Gua Sha and its underlying mechanism in rats with noncompressive lumbar disk herniation induced by autologous nucleus pulposus.

METHODS

A rat model of noncompressive lumbar disk herniation was established and rats were randomly divided into model group, sham group, and Gua Sha group (24 in each group). Gua Sha was performed from the 5th day after the surgery, once every other day, 3 times for a course of treatment, and totally 3 courses. The thermal withdrawal latency was evaluated using the intelligent hot plate one day before the surgery, and on days 4 (the day before the treatment), 10 (the end of the first course), 16 (the end of the second course) and 22 (the end of the third course). On days 4, 10, 16 and 22, six rats in each group were picked randomly and their blood samples were drawn to assess the expression of interleukin-1¦Â (IL-1¦Â), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-¦Á).

RESULTS

Compared to rats in the sham group, the application of nucleus pulposus to right L5 dorsal root ganglion induced prolonged thermal hyperalgesia, and up-regulated the expression of IL-1¦Â, IL-6 and TNF-¦Á in serum (P < 0.01). The therapy of Gua Sha attenuated thermal hyperalgesia potently, inhibited the expression of IL-1¦Â, IL-6 and TNF-¦Á in a time-dependent manner (P < 0.01). There were no significant differences in the thermal withdrawal latency and the expression of inflammatory cytokines between the sham and Gua Sha groups at the end of the treatment (P > 0.01).

CONCLUSION

The current study showed that Gua Sha might alleviate thermal hyperalgesia in rats with lumbar disc herniation induced by autologous nucleus pulposus via inhibiting the expression of proinflammatory cytokins.