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Breakthrough in drug-free pain relief: Solvent-mediated analgesia for safer, non-addictive pain management

Date:
December 11, 2024
Source:
National University of Singapore
Summary:
Researchers have made a discovery regarding the TRPV1 (transient receptor potential vanilloid 1) ion channel and its role in pain perception. The study reveals how solvent molecules can modulate pain signals, offering a potential pathway for a safer, non-addictive pain management approach.
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Researchers from the National University of Singapore (NUS), in collaboration with Peking University, China, have made a discovery regarding the TRPV1 (transient receptor potential vanilloid 1) ion channel and its role in pain perception. The study reveals how solvent molecules can modulate pain signals, offering a potential pathway for a safer, non-addictive pain management approach.

Pain management is a critical aspect of healthcare, directly impacting quality of life and overall well-being. The TRPV1 ion channel, essential for pain sensing, undergoes pore expansion when activated, allowing ions and larger molecules to pass through. However, the ability of water molecules to permeate the TRPV1 channel has remained uncertain.

To address this, the research team led by Professor LIU Xiaogang from the Department of Chemistry at NUS developed an upconversion nanoprobe capable of distinguishing between ordinary water (H₂O) and deuterated water (D₂O). This advanced technology enabled real-time tracking of water dynamics at both the single-cell and single-molecule levels. The study showed that when D₂O passed through the TRPV1 channel, it suppressed pain signal transmission and achieved effective analgesia. This research was conducted in collaboration with Professor Chao CHANG from Peking University and National Innovation Institute of Defense Technology, China, and also with Assistant Professor Bilin ZHUANG when she was with Yale-NUS College.

The findings were published in the journal Nature Biomedical Engineering.

Administering D₂O to pre-clinical models, the team successfully reduced both acute and chronic inflammatory pain transmission without affecting other neurological responses. This solvent-mediated analgesia mechanism provides an effective, biocompatible, and non-addictive alternative to traditional pain medications, circumventing issues related to drug dependency and tolerance.

Prof Liu said, "This discovery not only expands the scientific understanding of TRPV1 functionality but also opens new avenues for pain management. The research team aims to further explore the effects of D₂O on other ion channels, potentially applying this mechanism to treat neurological conditions and other medical challenges."

"The solvent-mediated analgesia mechanism represents an innovative breakthrough in pain relief, potentially driving the development of safer, non-addictive pain therapies for clinical use," added Prof Liu.


Story Source:

Materials provided by National University of Singapore. Note: Content may be edited for style and length.


Journal Reference:

  1. Yuxia Liu, Yuanyuan He, Jiahuan Tong, Shengyang Guo, Xinyu Zhang, Zichao Luo, Linlin Sun, Chao Chang, Bilin Zhuang, Xiaogang Liu. Solvent-mediated analgesia via the suppression of water permeation through TRPV1 ion channels. Nature Biomedical Engineering, 2024; DOI: 10.1038/s41551-024-01288-2

Cite This Page:

National University of Singapore. "Breakthrough in drug-free pain relief: Solvent-mediated analgesia for safer, non-addictive pain management." ScienceDaily. ScienceDaily, 11 December 2024. <www.sciencedaily.com/releases/2024/12/241211125052.htm>.
National University of Singapore. (2024, December 11). Breakthrough in drug-free pain relief: Solvent-mediated analgesia for safer, non-addictive pain management. ScienceDaily. Retrieved December 17, 2024 from www.sciencedaily.com/releases/2024/12/241211125052.htm
National University of Singapore. "Breakthrough in drug-free pain relief: Solvent-mediated analgesia for safer, non-addictive pain management." ScienceDaily. www.sciencedaily.com/releases/2024/12/241211125052.htm (accessed December 17, 2024).

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