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Paeoniflorin relieves LPS-induced inflammatory pain in mice by inhibiting NLRP3 inflammasome activation via transient receptor potential vanilloid 1.
- Source :
-
Journal of leukocyte biology [J Leukoc Biol] 2020 Jul; Vol. 108 (1), pp. 229-241. Date of Electronic Publication: 2020 Feb 21. - Publication Year :
- 2020
-
Abstract
- LPS has been widely used to induce inflammatory pain, attributing to production of inflammatory cytokines and sensitization of nociceptors. Paeoniflorin (PF) possesses anti-nociceptive property, but its effect on LPS-induced inflammatory pain has not been investigated. In this study, we aimed to investigate the analgesic effect of PF on an inflammatory pain mouse model and explore the underlying mechanisms. LPS-induced inflammatory pain model was established in C57BL/6J mice after PF treatment. Then, thermal hyperalgesia, neutrophil infiltration, inflammatory cytokine production, intracellular Ca <superscript>2+</superscript> levels, PKC activity, transient receptor potential vanilloid 1 (TRPV-1) expression, NF-κB transcription, and NLPR3 inflammasome activation were assessed by thermal withdrawal latency, histopathology, ELISA, intracellular Ca <superscript>2+</superscript> concentration, immunohistochemistry, and Western blot, separately. PF significantly relieved inflammatory pain and paw edema in mice with LPS-induced inflammatory pain. Additionally, PF inhibited neutrophil infiltration, inflammatory cytokine production (IL-1β, TNF-α, and IL-6), intracellular Ca <superscript>2+</superscript> levels, and PKC activity as well as suppressed TRPV-1 expression, NF-κB transcription, and NLPR3 inflammasome activation in the footpad tissue samples. Importantly, capsaicin (TRPV-1 agonists) obviously reversed the pain-relieving effect of PF, suggesting the involvement of TRPV-1 in the analgesic activity of PF. Our results indicated PF ameliorated LPS-induced inflammation and pain in mice by inhibiting TRPV-1-mediated NLRP3 inflammasome activation. These findings suggest that PF can be as a potential pharmacological agent for inflammatory pain and thus deserves more attention and further investigation.<br /> (©2020 Society for Leukocyte Biology.)
- Subjects :
- Animals
Calcium metabolism
Cytokines biosynthesis
Edema complications
Edema drug therapy
Glucosides pharmacology
Inflammasomes metabolism
Inflammation complications
Inflammation Mediators metabolism
Lipopolysaccharides
Macrophages drug effects
Macrophages metabolism
Male
Mice, Inbred C57BL
Models, Biological
Monoterpenes pharmacology
NF-kappa B genetics
NF-kappa B metabolism
NLR Family, Pyrin Domain-Containing 3 Protein metabolism
Neutrophils drug effects
Neutrophils pathology
Nociception drug effects
Pain complications
Protein Kinase C metabolism
TRPV Cation Channels agonists
Transcription, Genetic drug effects
Glucosides therapeutic use
Inflammasomes antagonists & inhibitors
Inflammation drug therapy
Monoterpenes therapeutic use
NLR Family, Pyrin Domain-Containing 3 Protein antagonists & inhibitors
Pain drug therapy
TRPV Cation Channels metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1938-3673
- Volume :
- 108
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Journal of leukocyte biology
- Publication Type :
- Academic Journal
- Accession number :
- 32083340
- Full Text :
- https://doi.org/10.1002/JLB.3MA0220-355R