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Electroacupuncture enhances antioxidative signal pathway and attenuates neuropathic pain induced by chemotherapeutic paclitaxel
X. Zhao, L. Liu, Y. Wang, G. Wang, Y. Zhao, Y. Zhang
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- antioxidancia * metabolismus MeSH
- elektroakupunktura metody MeSH
- fytogenní protinádorové látky toxicita MeSH
- krysa rodu rattus MeSH
- měření bolesti účinky léků metody MeSH
- neuralgie chemicky indukované metabolismus terapie MeSH
- paclitaxel toxicita MeSH
- potkani Sprague-Dawley MeSH
- signální transdukce účinky léků fyziologie MeSH
- spinální ganglia účinky léků metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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 F2alpha 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.
Department of Gerontology The 1st Hospital of Jilin University Changchun Jilin China
Department of Thoracic Surgery The 1st Hospital of Jilin University Changchun Jilin China
Division of Operation The 1st Hospital of Jilin University Changchun Jilin China
Jilin Heart Disease Hospital Changchun Jilin China
Tumor Center The 1st Hospital of Jilin University Changchun Jilin China
Citace poskytuje Crossref.org
Literatura
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