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Galangin, a novel Kv7 potassium channel opener, exerts potent antinociceptive effects in multiple chronic pain mouse models

Acta Pharmacologica Sinica (2025)Cite this article

Abstract

The activation of voltage-gated potassium Kv7/M channels is an attractive therapeutic strategy for chronic pain. Galangin, the principal active component of the medicinal herb Alpinia officinarum Hance, has exhibited analgesic effects in mice. In this study, we investigated the antinociceptive effects of galangin in the treatment of various types of chronic pain and the underlying mechanisms. Using whole-cell recordings of CHO cells expressing Kv7.2/Kv7.3 channels, we showed that galangin enhanced Kv7.2/Kv7.3 currents in a concentration-dependent manner, with an EC50 value of 8.8 ± 1.6 μM, and shifted the voltage-dependent activation curve of the channels toward depolarization. We demonstrated that galangin selectively and potently activated the Kv7.2, Kv7.4, and Kv7.5 channels while reducing the Kv7.1 current and exerting no effect on the Kv7.3 current. Notably, galangin no longer increased the current amplitude and slightly shifted the voltage-dependent activation of the Kv7.2 (E322A) mutant, suggesting that Glu-322 in Kv7.2 is important for galangin activation of the channels. Moreover, we showed that galangin (100 μM) significantly enhanced the M-current and consequently reduced the excitability of DRG neurons in SNI mice. In multiple chronic pain mouse models, the administration of galangin (15 mg/kg, i.p.) significantly increased the threshold for mechanical stimuli and the withdrawal latency to thermal stimuli, which were reversed by the Kv7/M channel blocker XE991. Taken together, the results of this study demonstrated that galangin exerts its antinociceptive effects mainly through the activation of Kv7/M channels, representing a novel approach for treating neuronal excitatory diseases.

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Fig. 1: Galangin enhances Kv7.2/Kv7.3 channel currents.
Fig. 2: Selectivity of galangin for the Kv7 channel subtype.
Fig. 3: Effects of galangin on the activation and deactivation kinetics of Kv7 subtypes.
Fig. 4: Amino acid binding site for galangin in the activation of the Kv7.2 channel.
Fig. 5: Effect of galangin on Kv7.2 mutant currents.
Fig. 6: Galangin enhances native M-currents and attenuates neuronal firing in DRG neurons.
Fig. 7: Galangin alleviates chronic pain induced by SNI, CFA, and MIA.

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Acknowledgements

This work was supported by STI 2030-Major Projects [Grant 2021ZD 0203200-04, China] (to FZ), the National Natural Science Foundation of China [Grant 32171018 and 32471066, China] (to FZ), the Natural Science Foundation of Hebei Province [Grant H2022206011 and C2024206032, China] (to FZ), and the Top Talent of Young People of Hebei Province (to FZ).

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  1. The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of Vascular Biology of Hebei Province, Department of Neurobiology, Hebei Medical University, Shijiazhuang, 050017, China

    Bo Yang, Hui Liu, Wen-jing Zhao, Jia-rui Ma, Zi-shuo Kang, Yu-jie Zhang, Yu-lin Gu, Xiao-ke Li, Zeng-wei Mao & Fan Zhang

  2. Department of Cardiology, Second Hospital of Hebei Medical University, Shijiazhuang, 050051, China

    Rui-feng Cao & Ya-ling Wang

  3. Department of Orthopaedic Surgery, Institute of Biomechanical Science and Biomechanical Key Laboratory of Hebei Province, Third Hospital of Hebei Medical University, Shijiazhuang, 050061, China

    Han Li

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Contributions

BY and Hui L conducted the pharmacological experiments, analyzed the data and wrote the paper. WJZ, JRM, ZSK and YJZ were involved in the animal experiments. YLG, XKL and ZWM analyzed the data. RFC and YLW edited and proofread the drafts and the final version of the article. FZ and Han L conceived/supervised the projects, designed the experiments, and revised the article.

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Yang, B., Liu, H., Zhao, Wj. et al. Galangin, a novel Kv7 potassium channel opener, exerts potent antinociceptive effects in multiple chronic pain mouse models. Acta Pharmacol Sin (2025). https://doi.org/10.1038/s41401-025-01627-2

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