Abstract | BACKGROUND: Up-regulation of CX3CL1 has been revealed to be involved in the neuropathic pain induced by nerve injury. However, whether CX3CL1 participates in the paclitaxel-induced painful peripheral neuropathy remains unknown. The aim of the current study was to elucidate the involvement of transcriptional factors nuclear factor-κB (NF-κB) and its causal interaction with CX3CL1 signaling in the paclitaxel-induced painful peripheral neuropathy. METHODS: Painful peripheral neuropathy induced by paclitaxel treatment was established in adult male Sprague-Dawley rats. The von Frey test were performed to evaluate neuropathic pain behavior, and real-time quantitative reverse transcription polymerase chain reaction, chromatin immunoprecipitation, Western blot, immunohistochemistry, and small interfering RNA were performed to understand the molecular mechanisms. RESULTS: CONCLUSIONS:
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Authors | Dai Li, Zhen-Zhen Huang, Yun-Zhi Ling, Jia-You Wei, Yu Cui, Xiang-Zhong Zhang, He-Quan Zhu, Wen-Jun Xin |
Journal | Anesthesiology
(Anesthesiology)
Vol. 122
Issue 5
Pg. 1142-51
(May 2015)
ISSN: 1528-1175 [Electronic] United States |
PMID | 25494456
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents, Phytogenic
- Chemokine CX3CL1
- Cx3cl1 protein, rat
- Cytokines
- Histones
- NF-kappa B
- Pyrrolidines
- RNA, Small Interfering
- Thiocarbamates
- Transcription Factor RelA
- pyrrolidine dithiocarbamic acid
- Paclitaxel
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Topics |
- Acetylation
- Animals
- Antineoplastic Agents, Phytogenic
(adverse effects)
- Chemokine CX3CL1
(biosynthesis, genetics)
- Cytokines
(biosynthesis)
- Histones
(metabolism)
- Hyperalgesia
(chemically induced, genetics)
- Male
- NF-kappa B
(antagonists & inhibitors, biosynthesis, genetics)
- Paclitaxel
(adverse effects)
- Pain Measurement
(drug effects)
- Peripheral Nervous System Diseases
(chemically induced, genetics, metabolism)
- Pyrrolidines
(pharmacology)
- RNA, Small Interfering
(pharmacology)
- Rats
- Rats, Sprague-Dawley
- Spinal Cord
(drug effects, metabolism)
- Thiocarbamates
(pharmacology)
- Transcription Factor RelA
(antagonists & inhibitors, biosynthesis, genetics)
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