title: Luteolin ameliorates dextran sulfate sodium-induced colitis in mice possibly through activation of the Nrf2 signaling pathway.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  These observations indicate that luteolin may suppress experimental colitis through the Nrf2 signaling pathway.
authors: Department of Gastroenterology, Key Laboratory of Hubei Province for Digestive System Disease, Renmin Hospital of Wuhan University, Wuhan, China. Electronic address: yzejy@126.com.
authors: Yue
authors: Y
authors: Li
authors: Department of Gastroenterology, Key Laboratory of Hubei Province for Digestive System Disease, Renmin Hospital of Wuhan University, Wuhan, China. Electronic address: 594158761@qq.com.
authors: Lei
authors: L
authors: Shen
authors: Department of Gastroenterology, Key Laboratory of Hubei Province for Digestive System Disease, Renmin Hospital of Wuhan University, Wuhan, China.
authors: Hesheng
authors: H
authors: Luo
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D002374:Catalase / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D003106:Colon / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D016264:Dextran Sulfate; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics; D047311:Luteolin / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D008810:Mice, Inbred C57BL; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000235:genetics / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015850:Interleukin-6; D008565:Membrane Proteins; D051267:NF-E2-Related Factor 2; C495636:Nfe2l2 protein, mouse; D014409:Tumor Necrosis Factor-alpha; C577686:interleukin-6, mouse; D008315:Malondialdehyde; D016264:Dextran Sulfate; D002374:Catalase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse; D013482:Superoxide Dismutase; D016660:NAD(P)H Dehydrogenase (Quinone); C491732:Nqo1 protein, mouse; D047311:Luteolin
keywords: DSS-induced colitis; HO-1; Luteolin; MDA; Nrf2; iNOS