Inhibition of inducible nitric oxide synthase and cyclooxygenase-2 expression by flavonoids isolated from Tanacetum microphyllum.

Plant flavonoids show anti-inflammatory activity both in vitro and in vivo. Some flavonoids have been reported previously to inhibit nitric oxide (NO) and prostaglandin E2 (PGE2) production by suppressing inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. The present study focuses on the effect of various naturally occurring flavonoids (santin, ermanin, centaureidin and 5,3'-dihydroxy-4'-methoxy-7-methoxycarbonylflavonol) on modulation of lipopolysaccharide (LPS)-induced iNOS and COX-2 expression in RAW 264.7 cells. Western blotting showed that all flavonoids suppressed the induction of both iNOS and COX-2. Ermanin and 5,3'-dihydroxy-4'-methoxy-7-methoxycarbonylflavonol were the most potent inhibitors. This study suggests that inhibition of iNOS and COX-2 expression by flavonoids may be one of the mechanisms responsible for their anti-inflammatory effects, and that they may be potential agents for use in the treatment of inflammatory diseases.

Quercetin, a flavonoid antioxidant, prevents and protects against ethanol-induced oxidative stress in mouse liver.

This study evaluates whether quercetin (25, 50 and 75 mg/kg body weight) treatment has a protective effect on the pro-oxidant-antioxidant state following chronic ethanol treatment in mice. Pretreatment (quercetin 25, 50 and 75 mg/kg body weight for 15 d+co-treatment of ethanol 18%+quercetin for 15 d and ethanol 18% for the 15 d) increased the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH) in comparison to the ethanol group. No significant differences from the ethanol group were observed in the group after post-treatment (ethanol 18% for 30 d+quercetin 25, 50 and 75 mg/kg body weight for 15 d) with quercetin. A significant increase in lipid peroxidation (malondialdehyde, MDA) products was observed in liver tissue after administration of ethanol, which was attenuated by pre- and post-treatment with a high dose of quercetin. GSH levels increased and oxidized glutathione (GSSG) levels decreased in groups of ethanol-exposed mice that received quercetin for 15 d prior to ethanol exposure. In conclusion, pre-treatment of quercetin may protect against ethanol-induced oxidative stress by directly quenching lipid peroxides and indirectly by enhancing the production of the endogenous antioxidant GSH. There was no protective effect on post-treatment with quercetin.