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Updated: Jul 16, 2026

Human In-Vivo Bioassay for the Tissue-Specific Measurement of Nociceptive and Inflammatory Mediators
Published on: December 1, 2008
Hydrogen sulfide as a novel nociceptive messenger
Atsufumi Kawabata1, Tsuyoshi Ishiki, Keita Nagasawa
1Division of Physiology and Pathophysiology, Department of Pharmacy, School of Pharmacy, Kinki University, Higashi-Osaka 577-8502, Japan. kawabata@phar.kindai.ac.jp
Hydrogen sulfide (H2S) acts as a pain messenger by sensitizing T-type calcium channels, contributing to hyperalgesia, especially during inflammation.
Area of Science:
- Biochemistry
- Neuroscience
- Pharmacology
Background:
- Hydrogen sulfide (H2S) is an endogenous gasotransmitter involved in mammalian biological events, including inflammation.
- The role of H2S in peripheral pain processing remains to be fully elucidated.
Purpose of the Study:
- To investigate the involvement of H2S in peripheral nociceptive processing.
- To explore the mechanisms underlying H2S-induced hyperalgesia.
Main Methods:
- Administration of H2S donor (NaHS) and L-cysteine in rats to induce hyperalgesia.
- Inhibition of H2S-evoked hyperalgesia using specific inhibitors (DTNB, ethosuximide, mibefradil, PPG, BCA).
- Patch-clamp electrophysiology on NG108-15 cells to assess T-type Ca2+ channel activity.
Main Results:
- Intraplantar administration of NaHS induced hyperalgesia and Fos expression in the spinal dorsal horn.
- H2S-evoked hyperalgesia was blocked by T-type Ca2+ channel inhibitors and an oxidizing agent.
- Inhibition of H2S synthesis reduced lipopolysaccharide-induced hyperalgesia, which was reversed by NaHS.
- NaHS enhanced T-type Ca2+ channel currents in NG108-15 cells.
Conclusions:
- Hydrogen sulfide acts as a novel nociceptive messenger in peripheral tissues.
- H2S sensitizes T-type Ca2+ channels, contributing to pain signaling, particularly during inflammatory conditions.
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