Antinociceptive and anti-inflammatory effects of myricetin 3-O-β-galactoside isolated from Davilla elliptica: involvement of the nitrergic system

Abstract

We aimed to study the antinociceptive effects of myricetin 3-O-β-galactoside (Mi), a substance isolated from the hydroalcoholic extract of Davilla elliptica. This study examined male Swiss mice, inducible nitric oxide synthase C57B16/J knockout mice (iNOS(-/-)), and their corresponding wild type (WT). Formalin and tail-flick tests were used to evaluate the nociceptive threshold, and the carrageenan-induced paw edema test was used as a model for inflammation. The following drugs were administered to investigate the involvement of the nitrergic and opioidergic systems: L-NAME, a nonspecific nitric oxide synthase (NOS) inhibitor; L-arginine (L-Arg), a precursor for the synthesis of nitric oxide (NO); D-arginine (D-Arg), an inactive isomer for the synthesis of NO; aminoguanidine (Am), an inducible nitric oxide synthase (iNOS) inhibitor; and naloxone, a nonselective antagonist of opioid receptors. The results showed that oral pretreatment with Mi caused a dose-dependent inhibition of the inflammatory phase of the formalin test and did not alter motor performance. Intraperitoneal injection of L-NAME caused a reduction in the licking time during the second phase of the formalin test. The administration of L-Arg (but not D-Arg) reversed the antinociceptive effect of L-NAME. Furthermore, pre-administration of aminoguanidine potentiated the antinociceptive effect. Mi did not cause an antinociceptive effect in iNOS knockouts and led to a reduction in the nitrite concentration in the paws of mice. Carrageenan-induced paw edema was reduced in Swiss mice and WT mice when compared to iNOS(-/-) mice. Pre-administration of naloxone (NLX) did not reverse the antinociceptive effect of Mi, excluding the opioidergic system as a mediator of the antinociceptive effect. Thus, the results suggest that the antinociceptive and anti-inflammatory effects of myricetin 3-O-β-galactoside are related to peripheral inhibition of nitric oxide synthesis, mainly iNOS.

Myricetin ameliorates atherosclerosis in the low-density-lipoprotein receptor knockout mice by suppression of cholesterol accumulation in macrophage foam cells

“…The main purpose of this study was to evaluate the effect of myricetin on atherosclerotic development using Ldlr −/− mice. Myricetin is a narurally occuring flavonoid and the anti-inflammation effect of myricetin has well been established [19, 20]. However, the efficacy of myricetin on atherogenesis and the mechanism ramained elusive.…”

Myricetin: A comprehensive review on its biological potentials

“…This decline of intracellular calcium hindering the release of neurotransmitters especially substance P, which are responsible for central analgesic effect. It was concluded that the anti-inflammatory and antinociceptive effects of myricetin could be imputable to the inhibition of iNOS (de Oliveira Azevedo et al, 2015). Mouse bone marrow (LPS-stimulated)-derived dendritic cells (DCs) treated with 10 µg/ml myricetin resulted in a significant reduction in TNFα secretion, IL-12 and IL-6.…”

“…This decline of intracellular calcium hindering the release of neurotransmitters especially substance P, which are responsible for central analgesic effect. It was concluded that the anti‐inflammatory and antinociceptive effects of myricetin could be imputable to the inhibition of iNOS (de Oliveira Azevedo et al., 2015 ).…”

Traditional Uses, Phytochemistry, and Pharmacology of Elegia Species: A Review

“…Myricetin 3-galactoside (5) and myricetin 3-rhamnoside (7) have shown in vitro antioxidant and antigenotoxic activity [22,23]. In addition, myricetin 3-galactoside (5) has demonstrated antinociceptive, anticatabolic and anti-inflammatory activities [24,25]. Recently, this compound has exhibited anti-osteoporotic properties [26].…”