Hydroxytyrosol ameliorates LPS-induced acute liver injury (ALI) in mice by modulating the balance between M1/M2 phenotype macrophage and inhibiting TLR4/NF-κB activation
[Display omitted] •Hydroxytyrosol is a phenolic compound found in the fruit and leaves of the olive.•Hydroxytyrosol ameliorated LPS-induced liver pathological morphology and decreased ALT and AST levels in mice.•Hydroxytyrosol inhibited overexpression of F4/80 and modulated the balance between M1/M2...
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Veröffentlicht in: | Journal of functional foods 2023-03, Vol.102, p.105455, Article 105455 |
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Sprache: | eng |
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•Hydroxytyrosol is a phenolic compound found in the fruit and leaves of the olive.•Hydroxytyrosol ameliorated LPS-induced liver pathological morphology and decreased ALT and AST levels in mice.•Hydroxytyrosol inhibited overexpression of F4/80 and modulated the balance between M1/M2 phenotype macrophage of LPS-induced acute liver injury in mice.•Hydroxytyrosol inhibited TLR4/NF-κB pathway activation of LPS-induced acute liver injury in mice.
Olive oil and olive leaves are essential components of the Mediterranean diet with well-established antioxidant and anti-inflammatory properties attributed to their high content of phenolic compounds, especially hydroxytyrosol (HT). Herein, we investigated whether HT exerts an anti-inflammatory effect on LPS-induced acute liver injury (ALI) in mice. Our data showed that HT ameliorated LPS-induced liver injury and decreased ALT and AST levels, with a more potent antioxidant capacity observed in the LPS + HT group than in the LPS group. HT inhibited LPS-induced overexpression of F4/80 and mRNA expression of M1 macrophage markers (TNF-α, IL-6 and IL-1β) and upregulated the mRNA levels of M2 macrophage markers (Mrc1, IL-10 and Arg1). HT downregulated the expression of mRNAs (TLR4, MyD88 and NF-κB) and proinflammatory factor proteins (TNF-α, IL-6 and IL-1β) associated with the TLR4/NF-κB pathway in LPS group. Overall, HT may modulate the balance between M1/M2 phenotype macrophage and inhibit TLR4/NF-κB activation. |
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ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2023.105455 |