Myricetin, a
flavonoid isolated from many edible vegetables and fruits, has multiple
biological effects, including anti-inflammatory and anti-
tumor effects.
Myricetin could inhibit mast cell degranulation in vitro, and it reduced the eosinophil content in bronchoalveolar lavage fluid (BALF) of
ovalbumin (OVA)-sensitized mice. However, it remains unclear whether
myricetin alleviates
airway hyperresponsiveness (AHR), airway
inflammation, and oxidative stress in
asthma. Here, we investigated whether
myricetin attenuated AHR, airway
inflammation, and eosinophil infiltration in lungs of asthmatic mice. Mice were sensitized with OVA, then injected intraperitoneally with
myricetin to investigate anti-inflammatory and
antioxidant effects of
myricetin. Moreover, we examined its effects on human bronchial epithelial BEAS-2B cells stimulated with TNF-α and
IL-4, in vitro.
Myricetin effectively mitigated eosinophil infiltration, AHR, and goblet cell
hyperplasia in lung, and it reduced Th2
cytokine expression in BALF from asthmatic mice.
Myricetin effectively promoted
glutathione and
superoxide dismutase productions and mitigated
malondialdehyde expressions in mice by promoting Nrf2/HO-1 expression.
Myricetin also reduced the production of proinflammatory
cytokines, eotaxins, and
reactive oxygen species in BEAS-2B cells.
Myricetin effectively suppressed
ICAM-1 expression in inflammatory BEAS-2B cells, which suppressed monocyte cell adherence. These results suggested that
myricetin could effectively improve
asthma symptoms, mainly through blocking Th2-cell activation, which reduced oxidative stress, AHR, and airway
inflammation.