Rapid induction of colorectal tumors in rats initiated with 1,2-dimethylhydrazine followed by dextran sodium sulfate treatment

Onose, Jun‐ichi; Imai, Toshio; Hasumura, Mai; Ueda, Makoto; Hirose, Masao

doi:10.1016/s0304-3835(03)00316-1

Cited by 25 publications

(35 citation statements)

References 23 publications

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“…У разі введення ДмГ у щурів виникають пух-лини, головним чином, у низхідному відділі ободової кишки, переважно з екзофітним ти-пом росту, що узгоджується з даними літератури [34]. Д1 та мі-1 у групі щурів з індукованими пухлинами під час застосування протягом 27 тижнів виявляють протипухлинну активність, зменшуючи загальну площу пухлинного ура-ження на 46 та 60% відповідно (рис.…”

Section: протипухлинна активність д1 та мі-1 за дмг-індукованого канцunclassified

Effect of dihydropyrrol and maleimide derivatives on the state of the liver and colon in normal rats and those with colorectal carcinogenesis induced by dimethylhydrazine

Kuznietsova¹,

Ov²,

Mo³

et al. 2013

Ukr.Biochem.J.

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Section: протипухлинна активність д1 та мі-1 за дмг-індукованого канцunclassified

Effect of dihydropyrrol and maleimide derivatives on the state of the liver and colon in normal rats and those with colorectal carcinogenesis induced by dimethylhydrazine

Kuznietsova¹,

Ov²,

Mo³

et al. 2013

Ukr.Biochem.J.

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“…As an animal model for colitis-related carcinogenesis described previously (Onose et al, 2003), male Crj: CD-1 (ICR) mice were given a single intraperitoneal administration of 15 mg/kg body weight of the genotoxic colonic carcinogen, DMH. This was followed by one week of oral exposure to a non-genotoxic carcinogen, DSS, at 2% in drinking water.…”

Section: Animalsmentioning

confidence: 99%

Triptolide downregulates Rac1 and the JAK/STAT3 pathway and inhibits colitis-related colon cancer progression

et al. 2009

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Triptolide, a diterpenoid triepoxide from the traditional Chinese medicinal herb Tripterygium wilfordii Hook. f., is a potential treatment for autoimmune diseases as well a possible anti-tumor agent. It inhibits proliferation of coloretal cancer cells in vitro and in vivo. In this study, its ability to block progress of colitis to colon cancer, and its molecular mechanism of action are investigated. A mouse model for colitis-induced colorectal cancer was used to test the effect of triptolide on cancer progression. Treatment of mice with triptolide decreased the incidence of colon cancer formation, and increased survival rate. Moreover, triptolide decreased the incidence of tumors in nude mice inoculated with cultured colon cancer cells dose-dependently. In vitro, triptolide inhibited the proliferation, migration and colony formation of colon cancer cells. Secretion of IL6 and levels of JAK1, IL6R and phosphorylated STAT3 were all reduced by triptolide treatment. Triptolide prohibited Rac1 activity and blocked cyclin D1 and CDK4 expression, leading to G1 arrest. Triptolide interrupted the IL6R-JAK/STAT pathway that is crucial for cell proliferation, survival, and inflammation. This suggests that triptolide might be a candidate for prevention of colitis induced colon cancer because it reduces inflammation and prevents tumor formation and development.

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“…It has reported that DMH is converted to its ultimate carcinogenic metabolite, diazonium ion (by NAD+-dependent dehydrogenase), which could elicit an oxidative stress and also produce tumors in the colon [6]. Since, multiple treatments with either DSS or DMH and a long-term experimental period are needed to induce CRC, some researchers have been studied the molecular mechanisms of colitis-mediated CRC in animal models using combination treatment with a non-genotoxic DSS and genotoxic colon carcinogen DMH [7][8][9]. In these contexts, we postulated that it is one of potential strategies for prevention of inflammatory colorectal carcinogenesis to block DSS/DMH-induced pathological symptoms by chemopreventive natural product in vivo.…”

Section: Introductionmentioning

confidence: 99%

Chemopreventive effect of plant originated glycoprotein on colitis-mediated colorectal cancer in A/J mice

Lee

Lim

2007

J Biomed Sci

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This study was carried out to investigate the chemopreventive effects of glycoprotein (UDN glycoprotein, 116-kDa) isolated from Ulmus davidiana Nakai on colitis-mediated colorectal cancer (CRC) in A/J mice. UDN glycoprotein intake significantly reduced the incidence and the multiplicity of colorectal tumors, induced by combination treatment with 10 mg/kg 1,2-dimethylhydrazine (DMH) and 2% dextran sodium sulfate (DSS). We found that the abnormal levels of lactate dehydrogenase (LDH), thiobarbituric acid reactive substances (TBARS), and nitric oxide (NO) were significantly suppressed in proportion to the concentration of UDN glycoprotein (0.01% and 0.02%) in the mice serum. In addition, consumption of UDN glycoprotein attenuated the activities of proliferating cell nuclear antigen (PCNA), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), and inhibited the DNA-binding activities of nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) in the mice colonic tissue. Interestingly, the results obtained from reverse transcription polymerase chain reaction (RT-PCR) assay showed that 0.02% UDN glycoprotein inhibited the expressions of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 mRNA in the mice. Collectively, these results suggest that UDN glycoprotein has chemopreventive activity via modulation of inflammation-related factors responsible for development of colitis-mediated CRC in A/J mice.

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Rapid induction of colorectal tumors in rats initiated with 1,2-dimethylhydrazine followed by dextran sodium sulfate treatment

Cited by 25 publications

References 23 publications

Effect of dihydropyrrol and maleimide derivatives on the state of the liver and colon in normal rats and those with colorectal carcinogenesis induced by dimethylhydrazine

Effect of dihydropyrrol and maleimide derivatives on the state of the liver and colon in normal rats and those with colorectal carcinogenesis induced by dimethylhydrazine

Triptolide downregulates Rac1 and the JAK/STAT3 pathway and inhibits colitis-related colon cancer progression

Chemopreventive effect of plant originated glycoprotein on colitis-mediated colorectal cancer in A/J mice

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