The inhibitory effect of quercitrin gallate on iNOS expression induced by lipopolysaccharide in Balb/c mice.
- Author:
Hyun Ye JO
1
;
Youngsoo KIM
;
Sang Yoon NAM
;
Beom Jun LEE
;
Yun Bae KIM
;
Young Won YUN
;
Byeongwoo AHN
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords: Balb/c mice; iNOS; lipopolysaccharide; quercitrin gallate
- MeSH: Animals; DNA Primers; Gene Expression Regulation, Enzymologic/drug effects; Lipopolysaccharides/*pharmacology; Liver/drug effects/enzymology; Mice; Mice, Inbred BALB C; Nitric Oxide/blood; Nitric Oxide Synthase Type II/drug effects/*genetics; Quercetin/*analogs & derivatives/pharmacology; RNA, Messenger/genetics; Reverse Transcriptase Polymerase Chain Reaction
- From:Journal of Veterinary Science 2008;9(3):267-272
- CountryRepublic of Korea
- Language:English
- Abstract: Quercetin 3-O-beta-(2''-galloyl)-rhamnopyranoside (QGR) is a naturally occurring quercitrin gallate, which is a polyphenolic compound that was originally isolated from Persicaria lapathifolia (Polygonaceae). QGR has been shown to have an inhibitory effect on nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated macrophage RAW 264.7 cells. Therefore, this study was conducted to investigate the inhibitory effect of QGR on nitric oxide production and inducible nitric oxide synthases (iNOS) expression in LPS-stimulated Balb/c mice. To accomplish this, 10 mg/kg of QGR was administered via gavage once a day for 3 days. iNOS was then induced by intraperitoneal injection of LPS. Six hours after the LPS treatment the animals were sacrificed under ether anethesia. The serum levels of NO were then measured to determine if QGR exerted an inhibitory effect on NO production in vivo. LPS induced an approximately 6 fold increase in the expression of NO. However, oral administration of QGR reduced the LPS induced increase in NO by half. Furthermore, RT-PCR and western blot analysis revealed that the increased levels of iNOS expression that occurred in response to treatment with LPS were significantly attenuated in response to QGR pretreatment. Histologically, LPS induced the infiltration of polymorphonuclear neutrophils in portal veins and sinusoids and caused the formation of a large number of necrotic cells; however, pretreatment with QGR attenuated these LPS induced effects. Taken together, these results indicate that QGR inhibits iNOS expression in vivo as well as in vitro and has antiinflammatory potentials.
