Quercetin Alleviates Chronic Post-Ischemia Pain in Rats and Inhibits NaV1.7 Sodium Channels
5 affiliations
- 1College of Chemistry and Environmental Engineering, Shenzhen University, Shenzhen 518055, China
- 2Health Science Center, Shenzhen University, Shenzhen 518055, China
- 3Department of Anatomy and Histology, Shenzhen University Medical School, Shenzhen 518055, China
- 4Department of Anesthesiology, Shenzhen People’s Hospital, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen 518020, China
- 5Department of Medical Neuroscience, School of Medicine, Shenzhen People’s Hospital, The First Affiliated Hospital, Southern University of Science and Technology, Shenzhen 518055, China
Abstract
Complex Regional Pain Syndrome type I (CRPS-I) poses a formidable challenge in pain management due to its debilitating symptoms and a lack of effective, targeted therapies. The chronic post-ischemia pain (CPIP) rodent model, which recapitulates the ischemia–reperfusion injury implicated in CRPS-I, provides a robust platform for exploring novel interventions. While quercetin (Que), a natural flavonoid, is recognized for its anti-inflammatory and antioxidant properties, its specific therapeutic efficacy and molecular targets in CRPS-I remain largely unknown. In this study, we evaluated the therapeutic potential of Que in addressing CRPS-related neuropathic pain using the CPIP model. Behavioral assessments revealed that Que significantly attenuates mechanical allodynia and cold hypersensitivity in CPIP rats. To elucidate the underlying mechanism, we investigated Que’s impact on peripheral nociceptive signaling. Whole-cell patch-clamp recordings demonstrated that Que markedly suppresses tetrodotoxin-sensitive (TTX-S) sodium currents in isolated dorsal root ganglion (DRG) neurons. To pinpoint the exact molecular target, we further evaluated Que in a heterologous expression system, confirming that it selectively inhibits Nav1.7 channel currents in transfected HEK293 cells. In addition to its known anti-inflammatory profile, our in vitro findings reveal that Que selectively modulates the Nav1.7 channel, providing new insights into its pleiotropic pharmacological characteristics. By bridging macroscopic analgesic phenotypes with a microscopic channel-blocking mechanism, this study establishes Que as a promising, safe, non-opioid candidate for CRPS-I translational therapy.
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BibTeX
@article{liu2026quercetin,
title = {{Quercetin Alleviates Chronic Post-Ischemia Pain in Rats and Inhibits NaV1.7 Sodium Channels}},
author = {Xiao Liu and Tao Liu and Weihang Zhao and Weijie Guo and Haoyi Yang and Jia Chen and Zhiming Shan and Song Cai},
journal = {Molecules},
year = {2026},
month = oct,
doi = {10.3390/molecules31213809},
url = {https://www.mdpi.com/1420-3049/31/21/3809},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Quercetin Alleviates Chronic Post-Ischemia Pain in Rats and Inhibits NaV1.7 Sodium Channels
AU - Xiao Liu
AU - Tao Liu
AU - Weihang Zhao
AU - Weijie Guo
AU - Haoyi Yang
AU - Jia Chen
AU - Zhiming Shan
AU - Song Cai
PY - 2026
DA - 2026/10/22
JO - Molecules
DO - 10.3390/molecules31213809
UR - https://www.mdpi.com/1420-3049/31/21/3809
AB - Complex Regional Pain Syndrome type I (CRPS-I) poses a formidable challenge in pain management due to its debilitating symptoms and a lack of effective, targeted therapies. The chronic post-ischemia pain (CPIP) rodent model, which recapitulates the ischemia–reperfusion injury implicated in CRPS-I, provides a robust platform for exploring novel interventions. While quercetin (Que), a natural flavonoid, is recognized for its anti-inflammatory and antioxidant properties, its specific therapeutic efficacy and molecular targets in CRPS-I remain largely unknown. In this study, we evaluated the therapeutic potential of Que in addressing CRPS-related neuropathic pain using the CPIP model. Behavioral assessments revealed that Que significantly attenuates mechanical allodynia and cold hypersensitivity in CPIP rats. To elucidate the underlying mechanism, we investigated Que’s impact on peripheral nociceptive signaling. Whole-cell patch-clamp recordings demonstrated that Que markedly suppresses tetrodotoxin-sensitive (TTX-S) sodium currents in isolated dorsal root ganglion (DRG) neurons. To pinpoint the exact molecular target, we further evaluated Que in a heterologous expression system, confirming that it selectively inhibits Nav1.7 channel currents in transfected HEK293 cells. In addition to its known anti-inflammatory profile, our in vitro findings reveal that Que selectively modulates the Nav1.7 channel, providing new insights into its pleiotropic pharmacological characteristics. By bridging macroscopic analgesic phenotypes with a microscopic channel-blocking mechanism, this study establishes Que as a promising, safe, non-opioid candidate for CRPS-I translational therapy.
SN - 1420-3049
ER -