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Hesperetin, a SIRT1 activator, inhibits hepatic inflammation via AMPK/CREB pathway
Ist Teil von
International immunopharmacology, 2020-12, Vol.89, p.107036-107036, Article 107036
Ort / Verlag
Amsterdam: Elsevier B.V
Erscheinungsjahr
2020
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
•Hesperetin suppresses NF-κB activity and LPS/D-GalN-induced hepatitis in mice.•Hesperetin inhibits NF-κB activity via enhancing RelA/p65 acetylation.•SIRT1 is required for the inhibitory effect of hesperetin on inflammation.•Hesperetin increases SIRT1 expression through AMPK/CREB pathway.
Silent mating type information regulation 2 homolog 1 (SIRT1) is an important inflammatory regulator, which epigenetically reprograms inflammation by altering the acetylation of NF-κB. Hesperetin, as a common flavonoid, has been proven to have a significant effect on acute inflammatory diseases. However, the detailed molecular mechanism by which hesperetin alleviates inflammatory response and accompanied tissue injury is poorly understood. Our results show that SIRT1 is required for the inhibitory effect of hesperetin on inflammation. Hesperetin suppresses the acetylation of RelA/p65 to reduce NF-κB activity by inducing SIRT1 expression. Mechanistically, hesperetin increases SIRT1 expression through AMPK/CREB pathway. Additionally, the protective effect of hesperetin against LPS/D-GalN-induced hepatitis in mice is also dependent on SIRT1. Our study suggests that hesperetin is an SIRT1 activator and could be potential candidates for the treatments of inflammatory conditions.