Methyl deficient diet aggravates experimental colitis in rats.
Bottom Line: Inflammatory bowel diseases (IBD) result from complex interactions between environmental and genetic factors.The mRNA levels of tumour necrosis factor (TNF)-α and protein levels of p38, cytosolic phospolipase A2 and cyclooxygenase 2 were significantly increased in the D DSS(+) pups and were accompanied by a decrease in the protein level of tissue inhibitor of metalloproteinases (TIMP)3, a negative regulator of TNF-α.MDD may cause an overexpression of pro-inflammatory pathways, indicating an aggravating effect of folate and/or vitamin B12 deficiency in experimental IBD.
Affiliation: Inserm U954, Medical faculty and CHU of Nancy, Nancy-Université, Nancy, France.Show MeSH
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Mentions: The mRNA level of TNF-α was determined by semi-quantitative real time RT-PCR, using PR29 (Ribosomal protein 29) as reference gene. The TNF-α mRNA level was significantly higher in colon from methyl-deficient rats compared to the rats fed a standard diet (Fig. 3). In line with the increased expression of TNF-α, Western blot analysis showed a decreased expression of TIMP3, a potent inhibitor of TNF-α in rats subjected to DSS and/or the MDD, compared with control animals. By contrast, expression levels of TACE were broadly similar between the four groups (Fig. 3). Western blot analysis revealed that the expression level of p38 was markedly increased by the MDD in the absence of DSS treatment (Fig. 4). The MDD dramatically increased the p38 protein level in DSS-treated rats, compared to animals receiving DSS alone (C/DSS+ group) (Fig. 4).
Affiliation: Inserm U954, Medical faculty and CHU of Nancy, Nancy-Université, Nancy, France.