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 methyl donor deficiency did not influence the mucosal thickness of the colon (0.26 ± 0.02, 0.22 ± 0.01 mm in C DSS− and D DSS− groups, respectively), while the DSS produced a significant reduction in the two DSS+ groups (0.17 ± 0.01 and 0.16 ± 0.02 mm in C DSS+ and D DSS+, respectively), compared with the other groups (P < 0.01). The absence of influence of the methyl donor deficiency on mucosal integrity was also demonstrated by the maintained expression of β-catenin and the absence of MPO in immunohistochemical examination of colon specimens from D DSS− rats, compared with C DSS− rats (Fig. 7). In agreement with these findings, the MPO activity was similar in colon samples of C DSS− and D DSS− rats (2.08 ± 0.55 and 1.67 ± 0.23 μmol/min./g, respectively).
Affiliation: Inserm U954, Medical faculty and CHU of Nancy, Nancy-Université, Nancy, France.