Curcumin inhibits trinitrobenzene sulphonic acid-induced colitis in rats by activation of peroxisome proliferator-activated receptor gamma

Zhang, Ming; Deng, Changsheng; Zheng, Jun; Xia, Jian Chuan; Shan, Dan

doi:10.1016/j.intimp.2006.02.013

Cited by 69 publications

(48 citation statements)

References 50 publications

(60 reference statements)

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“…These results are also consistent with other findings that showed a down-regulation by curcumin of COX-2 and iNOS transcription in other animal models [Ukil et al, 2003;Jiang et al, 2006;Zhang et al, 2006;Camacho-Barquero et al, 2007;Venkataranganna et al, 2007]. Furthermore, in vitro, curcumin inhibited COX-2 transcription in bile acid-and phorbol ester-treated human gastrointestinal epithelial cells [Zhang et al, 1999]; in macrophage-like differentiated RAW 264.7 cells [Atsumi et al, 2005]; in HT-29 human colon cancer cells [Goel et al, 2001]; in non-small cell lung carcinoma cells [Shishodia et al, 2003]; in Kupffer cells [Nanji et al, 2003], in microglial cells [Kang et al, 2004]; and in leukocytes from healthy volunteers [Plummer et al, 2001].…”

Section: Discussionsupporting

confidence: 93%

Protective effect of curcumin, a Curcuma longa constituent, in early colonic inflammation in rats

Sánchez-Calvo

Villegas

Sánchez-Fidalgo

et al. 2009

Drug Development Research

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Curcumin, a polyphenol derived from the plant, Curcuma longa, has a variety of pharmacological effects, including chemotherapeutic, anti-inflammatory, antiangiogenic, and antioxidant activities. To gain a better understanding of the effects and mechanisms of action of curcumin on the acute injury caused by intra-colonic administration of acetic acid (AA) in rats, inflammation was assessed by histology and myeloperoxidase activity (MPO; an index of neutrophil infiltration in the mucosa); Th1 and Th2 cytokine production; histological and histochemical analysis of the lesions; nitrite production in colon mucosa; and the expression of iNOS, COX-1 and -2 using Western blotting and inmmunohistochemistry. We also studied the involvement of the p38 MAPK/JNK signalling pathway in the protective effect of curcumin in acute colonic inflammation. Curcumin (50-100 mg/kg/day) reduced the degree of colonic injury, the index of neutrophil infiltration and Th1 cytokine secretion, and increased IL-10 production, reduced colonic levels of nitrites, and reduced COX-2 and iNOS overexpression. A reduction in the activation of p38 and JNK MAPKs was also observed. Thus, we show that the widely used food additive, curcumin reduced the development of AA-induced colitis and alleviated the inflammatory response. Inhibition of MAPK signalling by curcumin could explain the changes on the cytokine Th1/Th2 profile, the reduction of COX-2 and iNOS signaling, as well as the decreased nitrite production in colonic mucosa, suggesting that curcumin may be useful in the treatment of ulcerative colitis. Drug Dev Res 70 : 425-437, 2009.

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Section: Discussionsupporting

confidence: 93%

Protective effect of curcumin, a Curcuma longa constituent, in early colonic inflammation in rats

Sánchez-Calvo

Villegas

Sánchez-Fidalgo

et al. 2009

Drug Development Research

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“…Curcumin has been proved to inhibit the growth and differentiation of many cancer cell lines [28,29] . Administration of 30 mg/kg curcumin by intraperitoneal injection for 2 wk could significantly improve the expression of PPARγ in colonic tissues of rats [30] . To the best of our knowledge, the effects of curcumin on PPARδ have not been investigated.…”

Section: Discussionmentioning

confidence: 93%

Curcumin suppresses PPARδ expression and related genes in HT-29 cells

Wang¹,

Li²,

Zheng³

et al. 2009

WJG

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AIM:To investigate the effects of curcumin on the expression of peroxisome proliferator-activated receptorδ (PPARδ) and related genes in HT-29 cells. METHODS:HT-29 cells were treated with curcumin (0-80 μmol/L) for 24 h. The effects of curcumin on the morphology of HT-29 cells were studied by Hoechst 33342 staining. The activity of caspase-3 was determined using DEVD-p NA as substrate. The levels of peroxisome PPARδ, 14-3-3ε and vascular endothelial growth factor (VEGF) in HT-29 cells were determined by Western blotting analysis and their mRNA expression was determined by real-time quantitative RT-PCR. RESULTS:Treatment with 10-80 μmol/L curcumin induced typical features of apoptosis and activated the caspase-3 in HT-29 cells. The expression of PPARδ, 14-3-3ε and VEGF was reduced and the activity of β-catenin/Tcf-4 signaling was inhibited by curcumin treatment. CONCLUSION:Curcumin can induce apoptosis of HT-29 cells and down-regulate the expression of PPARδ, 14-3-3ε and VEGF in HT-29.

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“…These effects have been reported in many cell types, including intestinal epithelial cells (20), mac-rophages, dendritic cells, B cells, and T cells (17). The potential usefulness of curcumin in the treatment of IBD was suggested by studies in chemically induced rodent models of colitis (19,35,46,48,49,51,52). Curcumin has also been demonstrated as an effective agent in maintenance therapy of UC (15), and encouraging, though not conclusive, data were obtained in a small clinical trial in CD patients (16).…”

mentioning

confidence: 99%

Limited effects of dietary curcumin on Th-1 driven colitis in IL-10 deficient mice suggest an IL-10-dependent mechanism of protection

Larmonier¹,

Uno²,

Lee³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Curcumin inhibits trinitrobenzene sulphonic acid-induced colitis in rats by activation of peroxisome proliferator-activated receptor gamma

Cited by 69 publications

References 50 publications

Protective effect of curcumin, a Curcuma longa constituent, in early colonic inflammation in rats

Protective effect of curcumin, a Curcuma longa constituent, in early colonic inflammation in rats

Curcumin suppresses PPARδ expression and related genes in HT-29 cells

Limited effects of dietary curcumin on Th-1 driven colitis in IL-10 deficient mice suggest an IL-10-dependent mechanism of protection

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