Electroacupuncture enhances antioxidative signal pathway and attenuates neuropathic pain induced by chemotherapeutic paclitaxel

Title:

Electroacupuncture enhances antioxidative signal pathway and attenuates neuropathic pain induced by chemotherapeutic paclitaxel

Creator:

Zhao, Xiaoming, Liu, Li, Wang, Yuku, Wang, Gang, Zhao, Yingkai, and Zhang, Yao

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:edca70a3-0164-40aa-a9b8-b473de162b1b
uuid:edca70a3-0164-40aa-a9b8-b473de162b1b
doi:10.33549/physiolres.934084

Subject:

electroacupuncture, paclitaxel, neuropathic pain, Nrf2-ARE, SOD, and oxidative stress

Type:

model:article and TEXT

Format:

bez média and svazek

Description:

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.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Coverage:

501-510

Source:

Physiological research | 2019 Volume:68 | Number:3

Harvested from:

CDK

Metadata only:

false