Isorhamnetin‐3‐O‐Glucuronide Suppresses JNK and p38 Activation and Increases Heme‐Oxygenase‐1 in Lipopolysaccharide‐Challenged RAW264.7 Cells. Issue 3 (May 2016)

• Record Type: Journal Article
• Authors: Park, Jin‐Young; Kim, Song‐In; Lee, Hee Jae; Kim, Sung‐Soo; Kwon, Yong‐Soo; Chun, Wanjoo
• Is Part Of: Drug development research. Volume 77:Issue 3(2016)
• Page Start: 143
• Page End: 151
• Publication Date: 2016-05
• Subjects: isorhamnetin‐3‐O‐glucuronide -- RAW264.7 cells -- HO‐1 -- lipopolysaccharide -- inducible nitric oxide synthase -- cyclooxygenase‐2 -- c‐Jun N‐terminal kinase -- p38; Drug development -- Periodicals; Drugs -- Research -- Periodicals; 615.19
• DOI: 10.1002/ddr.21301
• Languages: English
• ISSNs: 0272-4391

Abstract

Abstract: Preclinical Research Isorhanmetin (ISH) exhibits a wide range of biological properties including anticancer, anti‐oxidant and anti‐inflammatory activities. However, the pharmacological properties of isorhamnetin ‐ 3 ‐O ‐glucuronide (IG), a glycoside derivative of ISH, have not been extensively examined. The objective of this study was to examine the anti‐inflammatory properties of IG and its underlying mechanism in lipopolysaccharide (LPS)‐challenged RAW264.7 macrophage cells in comparison with its aglycone, ISH. IG suppressed LPS‐induced extracellular secretion of the proinflammatory mediators, nitric oxide (NO) and PGE2, and proinflammatory protein expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase‐2. IG also increased expression of heme oxygenase‐1 (HO‐1). IG attenuated LPS‐induced activation of c‐Jun N‐terminal kinase (JNK) and p38 in a concentration‐dependent manner with negligible suppression of extracellular signal‐regulated kinases (ERK) phosphorylation. In conclusion, this study demonstrates that IG exerts anti‐inflammatory activity by increasing HO‐1 expression and by suppressing JNK and p38 signaling pathways in LPS‐challenged RAW264.7 macrophage cells. Drug Dev Res 77 : 143–151, 2016. © 2016 Wiley Periodicals, Inc.