Effects of Morin on an Experimental Model of Acute Colitis in Rats

Ma, Ocete; Gálvez, Júlio; Me, Crespo; Cruz, T.; González, María Paula; Mi, Torres; Zarzuelo, Antonio

doi:10.1159/000028250

Cited by 46 publications

(35 citation statements)

References 29 publications

(44 reference statements)

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“…the inflamed colon. Probably, higher concentrations should be needed in order to reach anti-inflammatory effects in the colon, such as that described with morin [37]. In contrast, the glycosylated form of quercetin is protected from absorption and reaches the last portion of the intestine intact and in high amounts.…”

Section: Discussionmentioning

confidence: 99%

In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

et al. 2005

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Quercetin is a common antioxidant flavonoid found in vegetables, which is usually present in glycosylated forms, such as quercitrin (3-rhamnosylquercetin). Previous in vitro experiments have shown that quercetin exerts a bigger effect than quercitrin in the down-regulation of the inflammatory response. However, such results have not been reproduced in in vivo experimental models of intestinal inflammation, in which quercetin did not show beneficial effects while its glycosides, quercitrin or rutin, have demonstrated their effectiveness. In this study, we have reported that the in vivo effects of quercitrin in the experimental model of rat colitis induced by dextran sulfate sodium can be mediated by the release of quercetin generated after glycoside's cleavage by the intestinal microbiota. This is supported by the fact that quercetin, but not quercitrin, is able to down-regulate the inflammatory response of bone marrow-derived macrophages in vitro. Moreover, we have demonstrated that quercetin inhibits cytokine and inducible nitric oxide synthase expression through inhibition of the NF-jB pathway without modification of c-Jun N-terminal kinase activity (both in vitro and in vivo). As a conclusion, our report suggests that quercitrin releases quercetin in order to perform its anti-inflammatory effect which is mediated through the inhibition of the NF-jB pathway.

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Section: Discussionmentioning

confidence: 99%

In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

et al. 2005

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“…Morin (2',3,4',5,7-pentahydroxyflavone, flavonol) is a yellowish pigment extractable from the wood of Chlorophora tinctoria and acts as a broad-spectrum and non-toxic antioxidant [89] . Our laboratory analyzed the effects of morin on experimental TNBS-induced IBD in rats.…”

Section: Flavonoidsmentioning

confidence: 99%

“…Oral administration of morin, at doses ranging from 10 to 200 mg/kg, significantly reduced the mucosal damage by 20%-40% induced by the TNBS experimental model of IBD, although these beneficial effects were not dose-related. Morin reduced the enzymatic activity of myeloperoxidase (MPO) (marker of neutrophil infiltration) and can be interpreted as a manifestation of this antiinflammatory property [89] . Also, significantly inhibited LTB4 synthesis, and this inhibition was maximal at the highest dose of morin assayed (200 mg/kg).…”

Section: Flavonoidsmentioning

confidence: 99%

Current view of the immunopathogenesis in inflammatory bowel disease and its implications for therapy

Torres¹,

Rı́os

2008

WJG

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A l t h o u g h t h e a e t i o l o g y o f i n f l a m m a t o r y b o w e l disease (IBD) remains unknown, the pathogenesis is gradually being unravelled, seeming to be the result of a combination of environmental, genetic, and immunological factors in which an uncontrolled immune response within the intestinal lumen leads to inflammation in genetically predisposed individuals. Multifactorial evidence suggests that a defect of innate immune response to microbial agents is involved in IBD. This editorial outlines the immunopathogenesis of IBD and their current and future therapy. We present IBD as a result of dysregulated mucosal response in the intestinal wall facilitated by defects in epithelial barrier function and the mucosal immune system with excessive production of cytokines growth factors, adhesion molecules, and reactive oxygen metabolites, resulting in tissue injury. Established and evolving therapies are discussed in the second part of this editorial and at the end of this section we review new therapies to modulate the immune system in patients with IBD.

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“…Flavonoids are excellent candidates because of their anti-inflammatory properties and their low toxicity. Several flavonoids have been shown to exert intestinal anti-inflammatory activity in vivo, including (mg/kg) quercitrin 1-5 (1) , rutin 10-25 (2) , morin 25 (3,4) , hesperidin and diosmin 10-25 (5) . However, the mechanism of action is unclear.…”

mentioning

confidence: 99%

“…, rutin 10-25 (2) , morin 25 (3,4) , hesperidin and diosmin 10-25 (5) . However, the mechanism of action is unclear.…”

mentioning

confidence: 99%

Polyphenols and immunity

Medina¹,

Zarzuelo²

2008

Proc. Nutr. Soc.

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Flavonoids are biologically-active polyphenolic compounds with antioxidative, antineoplasic, cardiovascular protective and antiinflammatory properties. Pharmacological therapy is essential in inflammatory bowel disease but has many adverse effects and does not cure the disease. Flavonoids are excellent candidates because of their anti-inflammatory properties and their low toxicity. Several flavonoids have been shown to exert intestinal anti-inflammatory activity in vivo, including (mg/kg) quercitrin 1-5 (1) , rutin 10-25 (2) , morin 25 (3,4) , hesperidin and diosmin 10-25 (5) . However, the mechanism of action is unclear. Since inflammation is associated by significant oxidative stress, this mechanism may be relevant. Indeed, flavonoid treatment counters colitis-induced glutathione depletion. On the other hand, quercitrin treatment reduces macrophage infiltration in the dextran sulfate sodium colitis model (6) . The effects of flavonoids on primary macrophages have been studied and their structure-activity relationship characterized (7) . A number of flavonoids inhibit macrophage proliferation (but not cell viability) and some additionally reduce TNF and inducible NO synthase (iNOS) expression, probably interfering with the NF-kB pathway. The structural determinants of activity include the C-2 --C-3 double bond, the catechol group in the B ring and the 2-position of the B ring.Most of these flavonoids are glycosides, which are known to be hydrolysed by bacterial enzymes in the gut. Since luteolin and quercetin are not active in vivo and aglycone flavonoids are absorbed in the small intestine it is likely that glycosides act as prodrugs, releasing the biologically-active aglycone in the lumen and preventing their premature absorption, which has been proven in the case of quercitrin (8) . In particular, a faecal homogenate was shown to mediate quercetin release from quercitrin in vitro, and the resulting aglycone retained TNF, iNOS and IL-1b inhibitory activity in murine bone marrow-derived macrophages. This principle probably applies to the other heterosides with known intestinal anti-inflammatory activity.In conclusion, flavonoids have intestinal anti-inflammatory activity that is associated with macrophage inhibition and antioxidative effects. Further investigation of the mechanistic aspects of flavonoid pharmacological action is underway.

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Effects of Morin on an Experimental Model of Acute Colitis in Rats

Cited by 46 publications

References 29 publications

In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

In vivo quercitrin anti‐inflammatory effect involves release of quercetin, which inhibits inflammation through down‐regulation of the NF‐κB pathway

Current view of the immunopathogenesis in inflammatory bowel disease and its implications for therapy

Polyphenols and immunity

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