Journal
CHEMICO-BIOLOGICAL INTERACTIONS
Volume 228, Issue -, Pages 88-99Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2015.01.011
Keywords
Hesperidin methyl chalcone; Pain; Inflammation; Cytokine; Oxidative stress; Nuclear factor-kappa B
Funding
- Brazilian Grants from Coordenadoria de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Ministerio da Ciencia, Tecnologia e Inovacao (MCTI)
- Secretaria da Ciencia, Tecnologia e Ensino Superior (SETI)/Fundacao Araucaria
- Governo do Estado do Parana
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Cytokines and reactive oxygen species are inflammatory mediators that lead to increased sensitivity to painful stimuli, and their inhibition represents a therapeutic approach in controlling acute and chronic pain. The water-soluble flavonone hesperidin methyl chalcone (HMC) is used in the treatment of venous diseases, but its bioactivity as anti-inflammatory and analgesic is poorly understood. The present study evaluated the protective effects of HMC in widely used mouse models of acute and prolonged inflammation and pain. Male Swiss mice were treated with HMC (3-100 or 30 mg/kg, intraperitoneally) or vehicle (saline) 1 h before inflammatory stimuli. In overt pain-like behavior tests, HMC inhibited acetic acid- and phenyl-p-benzoquinone-induced writhing, and capsaicin-, Complete Freund's Adjuvant (CFA)- and formalin-induced paw flinching and licking. HMC also inhibited carrageenan-, capsaicin- and CFA-induced mechanical and thermal hyperalgesia. Mechanistically, HMC inhibited carrageenan-induced cytokine (TNF-alpha, IL-beta, IL-6, and IL-10) production, oxidative stress and NF-kappa B activation. Furthermore, HMC did not cause gastric or hepatic injury in a 7 days treatment protocol. Thus, this is the first report that HMC reduces inflammation and inflammatory pain by targeting TRPV1 (transient receptor potential vanilloid type 1) receptor activity, oxidative stress, cytokine production, and NF-kappa B activity, which suggests its potential applicability in inflammatory diseases. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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