Limits...
Methyl deficient diet aggravates experimental colitis in rats.

Chen M, Peyrin-Biroulet L, George A, Coste F, Bressenot A, Bossenmeyer-Pourie C, Alberto JM, Xia B, Namour B, Guéant JL - J. Cell. Mol. Med. (2011)

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.

View Article: PubMed Central - PubMed

Affiliation: Inserm U954, Medical faculty and CHU of Nancy, Nancy-Université, Nancy, France.

Show MeSH

Related in: MedlinePlus

Histopathological examination of the haematoxylin- and eosin-stained colon specimens from methyl donor deficient rats (B) compared with controls (A). Immunohistochemistry of myeloperoxidase in colonic mucosa specimens from control (C) and methyl donor deficient rats (D). Immunohistochemistry of E-Cadherin in colonic mucosa of control (E) and methyl donor deficient rats (F). Data shown are representative of triplicate experiments and magnifications are indicated by bars.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3822959&req=5

fig07: Histopathological examination of the haematoxylin- and eosin-stained colon specimens from methyl donor deficient rats (B) compared with controls (A). Immunohistochemistry of myeloperoxidase in colonic mucosa specimens from control (C) and methyl donor deficient rats (D). Immunohistochemistry of E-Cadherin in colonic mucosa of control (E) and methyl donor deficient rats (F). Data shown are representative of triplicate experiments and magnifications are indicated by bars.

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).


Methyl deficient diet aggravates experimental colitis in rats.

Chen M, Peyrin-Biroulet L, George A, Coste F, Bressenot A, Bossenmeyer-Pourie C, Alberto JM, Xia B, Namour B, Guéant JL - J. Cell. Mol. Med. (2011)

Histopathological examination of the haematoxylin- and eosin-stained colon specimens from methyl donor deficient rats (B) compared with controls (A). Immunohistochemistry of myeloperoxidase in colonic mucosa specimens from control (C) and methyl donor deficient rats (D). Immunohistochemistry of E-Cadherin in colonic mucosa of control (E) and methyl donor deficient rats (F). Data shown are representative of triplicate experiments and magnifications are indicated by bars.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822959&req=5

fig07: Histopathological examination of the haematoxylin- and eosin-stained colon specimens from methyl donor deficient rats (B) compared with controls (A). Immunohistochemistry of myeloperoxidase in colonic mucosa specimens from control (C) and methyl donor deficient rats (D). Immunohistochemistry of E-Cadherin in colonic mucosa of control (E) and methyl donor deficient rats (F). Data shown are representative of triplicate experiments and magnifications are indicated by bars.
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).

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.

View Article: PubMed Central - PubMed

Affiliation: Inserm U954, Medical faculty and CHU of Nancy, Nancy-Université, Nancy, France.

Show MeSH
Related in: MedlinePlus