Luteolin ameliorates dextran sulfate sodium-induced colitis in mice possibly through activation of the Nrf2 signaling pathway

• Published in: International immunopharmacology Vol. 40; pp. 24 - 31
• Main Authors: Li, Yue, Shen, Lei, Luo, Hesheng
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.11.2016; Elsevier BV
• Subjects: Animals; Anti-Inflammatory Agents - pharmacology; Anti-Inflammatory Agents - therapeutic use; Antioxidants; Antioxidants - pharmacology; Antioxidants - therapeutic use; Catalase; Catalase - metabolism; Colitis; Colitis - chemically induced; Colitis - drug therapy; Colitis - metabolism; Colitis - pathology; Colon; Colon - drug effects; Colon - metabolism; Colon - pathology; Dextran; Dextran Sulfate; Drinking water; DSS-induced colitis; Heme; Heme oxygenase (decyclizing); Heme Oxygenase-1 - genetics; Heme Oxygenase-1 - metabolism; HO-1; Inflammatory bowel disease; Inflammatory bowel diseases; iNOS; Interleukin 6; Interleukin-6 - genetics; Intestine; Luteolin; Luteolin - pharmacology; Luteolin - therapeutic use; Male; Malondialdehyde; Malondialdehyde - metabolism; MDA; Membrane Proteins - genetics; Membrane Proteins - metabolism; Mice; Mice, Inbred C57BL; mRNA; NAD(P)H Dehydrogenase (Quinone) - genetics; NAD(P)H Dehydrogenase (Quinone) - metabolism; NADP; NF-E2-Related Factor 2 - genetics; NF-E2-Related Factor 2 - metabolism; Nitric oxide; Nitric Oxide Synthase Type II - metabolism; Nitric-oxide synthase; Nrf2; Oxidative stress; Oxygenase; Quinone oxidoreductase; Rodents; Scavenging; Signal transduction; Signal Transduction - drug effects; Sodium; Studies; Sulfates; Superoxide dismutase; Superoxide Dismutase - metabolism; Tumor Necrosis Factor-alpha - genetics; DSS-induced colitis; iNOS; HO-1; Luteolin; MDA; Nrf2
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2016.08.020

Luteolin has a reputation for being a safe and effective natural antioxidant that has strong radical scavenging and cell protective properties. The role of oxidative stress in inflammatory bowel disease (IBD) has been well established and is increasingly highlighted. Thus, we studied the protective effect of luteolin administration in a mouse model of experimental colitis. Experimental acute colitis was induced by administering 3% dextran sulfate sodium (DSS) in the drinking water of mice for 7days. The disease activity index (DAI); colon length; histological assessment; mRNA levels of nuclear factor-erythroid 2-related factor 2 (Nrf2), tumor necrosis factor (TNF-α), interleukin-6 (IL-6), heme oxygenase-1 (HO-1), and NADP(H): quinone oxidoreductase 1 (NQO-1); protein expression of Nrf2 and inducible nitric oxide synthase (iNOS); colon malondialdehyde (MDA) levels; and the activity levels of colonic superoxide dismutase (SOD) and catalase (CAT) were examined. Luteolin (20 and 50mg/kg) significantly attenuated the DAI, colon shortening and histological damage. In addition, luteolin administration effectively decreased the expression of inflammatory mediators, such as iNOS, TNF-α and IL-6. Luteolin also decreased the colonic content of MDA. The activities of colonic SOD and CAT and the levels of Nrf2 and its downstream targets, HO-1 and NQO1, were elevated by luteolin treatment. These observations indicate that luteolin may suppress experimental colitis through the Nrf2 signaling pathway. •Luteolin ameliorates dextran sulfate sodium-induced experimental colitis in mice.•The antioxidative and anti-inflammatory effects of luteolin on experimental colitis are proposed.•The mechanism may be through activating Nrf2 signaling pathway.