One of the significant limiting complications of paclitaxel is
painful peripheral neuropathy during its therapy for several types
of cancers. Our recent study showed that impairment of
Nrf2-antioxidant response element (Nrf2-ARE) and upregulation
of oxidative signals in the dorsal root ganglion (DRG) of rats with
treatment of paclitaxel result in neuropathic pain. The purpose of
this study was to examine the beneficial role played by
electroacupuncture (EA) in modifying neuropathic pain evoked by
paclitaxel via Nrf2-ARE and oxidative mechanisms. Behavioral
test was performed to determine mechanical and thermal
sensitivity in rats. Western Blot analysis and ELISA were used to
examine expression of Nrf2-ARE and superoxide dismutases
(SOD); and the levels of products of oxidative stress in the DRG.
Our data showed that paclitaxel increased mechanical and
thermal sensitivity and this was accompanied with impaired
Nrf2-ARE and SOD in the DRG and amplified products of
oxidative stress (i.e. 8-isoprostaglandin F2α and 8-hydroxy-2’-
deoxyguanosine). EA treatment largely restored the levels of
Nrf2-ARE/SOD and inhibited products of oxidative stress and
thereby attenuated mechanical and thermal hypersensitivity
induced by paclitaxel. In conclusion, we revealed specific
signaling pathways leading to paclitaxel-evoked neuropathic pain,
including impairment of Nrf2-ARE and heightened oxidative
signals. We further provided evidence for the role of EA in
alleviating paclitaxel-neuropathic pain via these molecular
mediators.