• Yukiko Matsumura, Yoshihito Yokoyama, Hachidai Hirakawa, Tatsuhiko Shigeto, Masayuki Futagami, and Hideki Mizunuma.
• Department of Obstetrics and Gynecology, Hirosaki Graduate School of Medicine, 5-Zaifu-cho, Hirosaki, Aomori 036-8562, Japan. yokoyama@cc.hirosaki-u.ac.jp.
• Mol Pain. 2014 Sep 21; 10: 61.

BackgroundThis study aimed to evaluate the prophylactic effect of goshajinkigan (GJG) on paclitaxel (PTX)-induced neuropathy and to elucidate the mechanism of action.ResultsThere 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.ConclusionsThese 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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