Naringenin reduces inflammatory pain in mice

Naringenin: an analgesic and anti-inflammatory citrus flavanone

“…High concentrations of naringenin reduces TRPV1 activation [7], which corroborates the naringenin inhibition of capsaicin-induced overt pain like-behavior and mechanical hyperalgesia [2]. At much lower concentrations compared to TRPV1, naringenin blocks TRPM3 ion channel, a noxious heat sensor channel [7].…”

“…The antioxidant activity is the most recognized effect of flavonoids, which depends, for instance, on hydrogen donation and electron stabilization in the phenolic rings [1]. Naringenin presents therapeutic effect in several models of inflammatory pain [2, 3, 5]. Naringenin inhibits the pain-like behavior induced by inflammatory stimuli such as phenyl-p-benzoquinone, acetic acid, formalin, complete Freund’s adjuvant, capsaicin, carrageenan [2], superoxide anion [3], and LPS [5].…”

“…Naringenin presents therapeutic effect in several models of inflammatory pain [2, 3, 5]. Naringenin inhibits the pain-like behavior induced by inflammatory stimuli such as phenyl-p-benzoquinone, acetic acid, formalin, complete Freund’s adjuvant, capsaicin, carrageenan [2], superoxide anion [3], and LPS [5]. Moreover, naringenin inhibits UVB irradiation-induced skin inflammatory edema, cytokine production, myeloperoxidase activity, matrix metalloproteinase-9 activity, and oxidative stress [4].…”

“…Activated macrophages and neutrophils induce oxidative stress by producing superoxide anion and other reactive oxygen (ROS) and nitrogen species. Naringenin inhibits leukocyte recruitment [2–5] and production of superoxide anion [3–5], whilst increases GSH [2–4], and antioxidant capacity [3–5]. Naringenin also acts on macrophages inducing Nrf2 activation, a nuclear factor that induces antioxidant and anti-inflammatory responses, inducing HO-1 expression [3].…”

“…Pro-hyperalgesic cytokines induce the production of lipid mediators such as PGE 2 that sensitize the nociceptor neurons. Naringenin inhibits LPS- and carrageenan-induced NFκB activation in vivo [2] and in vitro [5], which contributes to naringenin inhibition of IL-33 [2], TNFα [3–5], IL-1β [2, 4, 5] and IL-6 [4,5] production and expression of cyclooxygenase-2 mRNA [3] (Figure 1). …”