Abstract | BACKGROUND: This study aimed to evaluate the prophylactic effect of goshajinkigan (GJG) on paclitaxel (PTX)-induced neuropathy and to elucidate the mechanism of action. RESULTS: There was a time-dependent irreversible decrease in pain threshold in PTX group. In PTX/GJG group, pain threshold showed changes in the same level as control. Electron microscope showed that although the ganglion cells of control and PTX/GJG groups were normal, degeneration of the nucleus and swelling of the mitochondria were observed in PTX group. Expression of transient receptor potential vanilloid 4 (TRPV4) gene in PTX group significantly increased compared with that in control and PTX/GJG groups. In TRPV4 knock-out mice, no PTX-induced hyperalgesia was observed, and there was no significant difference in pain threshold between the 3 groups. CONCLUSIONS: These results showed that PTX induced hyperalgesia by enhancing TRPV4 expression, and suggested that GJG might alleviate hyperalgesia by preventing degeneration of the ganglion cells and suppressing TRPV4 expression.
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Authors | Yukiko Matsumura, Yoshihito Yokoyama, Hachidai Hirakawa, Tatsuhiko Shigeto, Masayuki Futagami, Hideki Mizunuma |
Journal | Molecular pain
(Mol Pain)
Vol. 10
Pg. 61
(Sep 21 2014)
ISSN: 1744-8069 [Electronic] United States |
PMID | 25240613
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents, Phytogenic
- Drugs, Chinese Herbal
- TRPV Cation Channels
- TRPV1 protein, mouse
- gosha-jinki-gan
- Paclitaxel
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Topics |
- Animals
- Antineoplastic Agents, Phytogenic
(toxicity)
- Cells, Cultured
- Disease Models, Animal
- Drug Administration Schedule
- Drugs, Chinese Herbal
(administration & dosage)
- Female
- Ganglia, Spinal
(cytology)
- Gene Expression Profiling
- Gene Expression Regulation
(drug effects, genetics)
- Hyperalgesia
(etiology, genetics, prevention & control)
- Mice
- Mice, Transgenic
- Mitochondria
(drug effects, pathology, ultrastructure)
- Paclitaxel
(toxicity)
- Pain Threshold
(drug effects, physiology)
- Peripheral Nervous System Diseases
(chemically induced, complications, pathology, prevention & control)
- Rats
- Rats, Inbred F344
- Sensory Receptor Cells
(drug effects, ultrastructure)
- TRPV Cation Channels
(deficiency, genetics)
- Time Factors
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