Goshajinkigan, a Traditional Japanese Medicine, Prevents Oxaliplatin-Induced Acute Peripheral Neuropath by Suppressing Functional Alteration of TRP Channels in Rat

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  • Mizuno Keita
    Tsumura Research Laboratories, Tsumura & Co., Japan
  • Kono Toru
    Center for Clinical and Biomedical Research, Sapporo Higashi Tokushukai Hospital, Japan Faculty of Pharmaceutical Sciences, Hokkaido University, Japan
  • Suzuki Yasuyuki
    Tsumura Research Laboratories, Tsumura & Co., Japan
  • Miyagi Chika
    Tsumura Research Laboratories, Tsumura & Co., Japan
  • Omiya Yuji
    Tsumura Research Laboratories, Tsumura & Co., Japan
  • Miyano Kanako
    Division of Cancer Pathophysiology, National Cancer Center Research Institute, Japan
  • Kase Yoshio
    Tsumura Research Laboratories, Tsumura & Co., Japan
  • Uezono Yasuhito
    Division of Cancer Pathophysiology, National Cancer Center Research Institute, Japan

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  • Goshajinkigan, a Traditional Japanese Medicine, Prevents Oxaliplatin-Induced Acute Peripheral Neuropathy by Suppressing Functional Alteration of TRP Channels in Rat

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The acute peripheral neuropathy induced by oxaliplatin treatment occurs very frequently and is aggravated by exposure to cold. Goshajinkigan (GJG), a traditional Japanese (kampo) medicine, was recently shown to be effective against oxaliplatin-induced acute neuropathy. However, because the effects of GJG and its mechanism in relation to those of its ingredients and its mechanism are not well understood, we examined the effects of GJG on acute neuropathy. Further, we investigated whether GJG affects the functions and gene expressions of transient receptor potential (TRP) channels using a rat model of oxaliplatin-induced neuropathy. Administration of oxaliplatin increased withdrawal responses from cold stimulation, and GJG or calcium gluconate/magnesium sulfate significantly inhibited the oxaliplatin-induced cold hypersensitivity. Application of menthol, a TRPA1/TRPM8 agonist, or allyl isothiocyanate (AITC), a selective TRPA1 agonist, to the hind paw of oxaliplatin-treated rats enhanced the nocifensive behaviors evoked by each agonist, whereas oxaliplatin had no significant effect on nocifensive behaviors evoked by capsaicin, a TRPV1 agonist. GJG treatment reduced menthol- or AITC-evoked withdrawal responses potentiated by oxaliplatin. Furthermore, GJG suppressed the increase of TRPA1 and TRPM8 mRNA expression induced by oxaliplatin in dorsal root ganglia. These findings suggest that GJG prevented oxaliplatin-induced acute peripheral neuropathy by suppressing functional alteration of TRP channels, especially TRPA1 and TRPM8.

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