Anti-oxidant Effects of Resveratrol on Mice with DSS-induced Ulcerative Colitis

Yao, Jun; Wang, Jianyao; Liu, Lei; Li, Yingxue; Xun, An-Ying; Zeng, Weisen; Jia, Chunhong; Wei, Xiaoxia; Feng, Jie; Zhao, Lei; Wang, Lisheng

doi:10.1016/j.arcmed.2010.05.002

Cited by 221 publications

(140 citation statements)

References 33 publications

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“…Given the fact that resveratrol has shown beneficial effects in many non-FA phenotypes, it appears unlikely that it acts in an FA-specific way. 47,48 Nonetheless, it partially normalized important hematopoietic parameters in our Fancd2 Ϫ/Ϫ mouse model and hence should be further pursued therapeutically.…”

Section: Discussionmentioning

confidence: 99%

Fancd2 −/− mice have hematopoietic defects that can be partially corrected by resveratrol

Zhang

Marquez-Loza

Eaton

et al. 2010

Blood

106

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Progressive bone marrow failure is a major cause of morbidity and mortality in human Fanconi Anemia patients. In an effort to develop a Fanconi Anemia murine model to study bone marrow failure, we found that Fancd2 ؊/؊ mice have readily measurable hematopoietic defects. Fancd2 deficiency was associated with a significant decline in the size of the c-Kit ؉ Sca-1 ؉ Lineage ؊ (KSL) pool and reduced stem cell repopulation and spleen colony-forming capacity. Fancd2 ؊/؊ KSL cells showed an abnormal cell cycle status and loss of quiescence. In addition, the supportive function of the marrow microenvironment was compromised in Fancd2 ؊/؊ mice. Treatment with Sirt1-mimetic and the antioxidant drug, resveratrol, maintained Fancd2 ؊/؊ KSL cells in quiescence, improved the marrow microenvironment, partially corrected the abnormal cell cycle status, and significantly improved the spleen colony-forming capacity of Fancd2 ؊/؊ bone marrow cells. We conclude that Fancd2 ؊/؊ mice have readily quantifiable hematopoietic defects, and that this model is well suited for pharmacologic screening studies. IntroductionFanconi anemia (FA) is a rare, autosomal, recessive genetic disorder associated with severe birth defects, cancer predisposition, and bone marrow failure. Thirteen causative genes (FANCA, FANCB, FANCC, FANCD1/BRCA2, FANCD2, FANCE, FANCF, FANCG/XRCC9, FANCI, FANCL/PHF9/Pog, FANCJ/BRIP1/BACH1, FANCM/Hef, and FANCN/ PALB2) have been identified and cloned to date, and the encoded proteins are believed to work together in a common DNA damageresponse pathway to maintain genomic integrity and protect the genome from DNA damage induced by cross-linking agents. 1,2 Although deficiency in DNA cross-link repair renders all FA cells susceptible to cross-linking agents, bone marrow is the most affected organ system. Mutations in any of the different FA genes almost universally lead to bone marrow failure, which is the primary cause of mortality in FA. 3 The pathogenesis of bone marrow failure in FA remains elusive. Mutations in several genes involved in DNA damage repair, including Atr, XPD, and Ercc1, caused either hematopoietic stem cell (HSC) loss or impaired HSC function under conditions of stress. [4][5][6] These studies suggest that the maintenance of genome integrity is critical for HSC survival and function. However, the extent to which genotoxicity, resulting from impaired DNA damage repair, contributes to bone marrow failure in FA is unclear. 7 Other pathways associated with hematopoietic failure, such as altered cytokine signaling, may also contribute to FA pathogenesis. 8,9 For example, levels of proapoptotic cytokines tumor necrosis factor-␣ (TNF-␣) and interferon-␥ (IFN-␥) are elevated in FA lymphocytes, bone marrow cells, and FA patient serum samples. 10-12 FA bone marrow cells (at least of the C complementation group) are also hypersensitive to these cytokines and undergo apoptosis when exposed to even low levels of them. [13][14][15] To better understand FA, multiple murine knockout models, includingand Fancl Ϫ/Ϫ m...

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Section: Discussionmentioning

confidence: 99%

Fancd2 −/− mice have hematopoietic defects that can be partially corrected by resveratrol

Zhang

Marquez-Loza

Eaton

et al. 2010

Blood

106

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“…iNOS was overexpressed and ROS-producing cells were increased in the lamina propria of IBD patients (25). Antioxidants provided protection against DSS-induced colitis (26). Whether anti-OXZ-colitis activity is mediated by ROS-scavenging requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

Tetramethylpyrazine attenuates PPAR-γ antagonist-deteriorated oxazolone-induced colitis in mice

Zheng

Yang

et al. 2011

Mol Med Report

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Abstract. Tetramethylpyrazine (TMP) is suggested to have anti-inflammatory activity. The aim of this study was to determine the role of peroxisome proliferator activated receptor γ (PPAR-γ) signaling in the pharmacologic effect of TMP on oxazolone (OXZ)-induced colitis. TMP (80 mg/kg/day i.p.) was administered daily 48 h after intrarectal instillation of OXZ, with or without PPAR-γ inhibitor [bisphenol A diglycidyl ether (BADGE) 30 mg/kg] during the 4 days before sacrifice. The inflammatory response was assessed by the disease activity index, macroscopy, histology and myeloperoxidase (MPO) activity. Expression levels of PPAR-γ, NF-κB p65, COX-2, iNOS and TNF-α mRNA in colon mucosa were determined by FQ-PCR, levels of PPAR-γ and NF-κB p65 protein were analyzed by immunohistochemistry, and the total and phosphorylated levels of p38 MAPK were assessed by western blotting. TMP significantly attenuated the damage caused by OXZ and substantially reduced the rise in MPO activity, TNF-α, iNOS, NF-κB p65 and COX-2 expression, as well as the increase in PPAR-γ production; however, no changes in the activation of p38 MAPK were observed. Inhibition of PPAR-γ signaling aggravated inflammation of colon mucosa, and increased p38 phosphrylation. TMP counteracted the effect of inhibition of PPAR-γ. We suggest that the effect of TMP treatment in ulcerative colitis may be related to PPAR-γ signaling, but is independent of PPAR-γ.

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“…The exact etiology of colitis is still not completely understood. However, several factors were suggested to be involved in the pathogenesis of colitis such as overgrowth of pathogenic microorganisms, overproduction of pro-inflammatory cytokines, formation of reactive oxygen species (ROS) and neutrophil infiltration [4]. Many compounds had been reported to induce colitis in animals such as dextran sodium sulphate (DSS) and TNBS [1].…”

Section: Discussionmentioning

confidence: 99%

“…The disease may be triggered in a susceptible person by environmental factors [2]. Several studies reported that the increased production of proinflammatory cytokines such as TNF-α and interleukin 10 as well as oxidative stress may have an important role in the pathogenesis of colitis [3][4][5]. Colitis is treated as an autoimmune disease.…”

Section: Introductionmentioning

confidence: 99%

“…These mediators not only amplify the immune and inflammatory response, but also have direct effects on epithelial function, on endothelial function and on repair mechanisms, thus increasing collagen synthesis. In addition, many of the cytokines (interleukins 1 and 6, TNF-α) will activate an acute phase response, resulting in fever and a rise in serum acute phase proteins [4].…”

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Ameliorative Potential of Minocycline and/or Lactulose on Experimentally Induced Colitis

Kabel

2016

IJPPE

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Abstract.Objective: The aim of this study was to compare between the effect of minocycline or lactulose alone and in combination on experimentally-induced colitis in rats. Materials and methods: Seventy albino rats were divided into 7 equal groups: Control untreated group, trinitrobenzenesulphonic acid (TNBS) group, TNBS + lactulose group, lactulose group, TNBS + minocycline group, minocycline group and TNBS + lactulose+ minocycline group.

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Anti-oxidant Effects of Resveratrol on Mice with DSS-induced Ulcerative Colitis

Cited by 221 publications

References 33 publications

Fancd2 −/− mice have hematopoietic defects that can be partially corrected by resveratrol

Fancd2 −/− mice have hematopoietic defects that can be partially corrected by resveratrol

Tetramethylpyrazine attenuates PPAR-γ antagonist-deteriorated oxazolone-induced colitis in mice

Ameliorative Potential of Minocycline and/or Lactulose on Experimentally Induced Colitis

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