Isorhamnetin-3-O-Glucuronide Suppresses JNK and p38 Activation and Increases Heme-Oxygenase-1 in Lipopolysaccharide-Challenged RAW264.7 Cells

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• 作者：Jin-Young Park ; Song-In Kim ; Hee Jae Lee ; Sung-Soo Kim ; Yong-Soo Kwon and Wanjoo Chun
• 关键词：isorhamnetin-3-O-glucuronide ; RAW264.7 cells ; HO-1 ; lipopolysaccharide ; inducible nitric oxide synthase ; cyclooxygenase-2 ; c-Jun N-terminal kinase ; p38
• 刊名：Drug Development Research
• 出版年：2016
• 出版时间：May 2016
• 年：2016
• 卷：77
• 期：3
• 页码：143-151
• 全文大小：342K
• ISSN：1098-2299

文摘

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.