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[Expression of pro-inflammation cytokines and activation of nuclear factor kappab in the intestinal mucosa of mice with ulcerative colitis].
OBJECTIVE: To investigate the expression of pro-inflammation cytokines and activation of nuclear factor kappaB (NF-kappaB) in mouse models of ulcerative colitis.
METHODS: Mouse models of ulcerative colitis were established by oral administration of 5% dextran sulfate sodium for 7 d, and the expression of tumor necrosis factor (TNF)- alpha and interleukin (IL)-1beta in the intestinal mucosa were detected by semi-quantitative reverse transcriptional (RT) PCR. The activation of NF-kappaB in the intestinal mucosa was evaluated by electrophoretic mobility shift assay (EMSA).
RESULTS: The expressions of TNF-alpha and IL-1beta were increased in the intestinal mucosa (P=0.009), and the nuclear binding activity of NF-kappaB was also up-regulated after the onset of colitis.
CONCLUSION: Pro-inflammatory cytokines play important roles in the pathogenesis of UC, and may exacerbate the inflammation of the intestinal mocosa and cause apoptosis of the epithelial cells, possibly under the regulation of NF-kappaB activation.
METHODS: Mouse models of ulcerative colitis were established by oral administration of 5% dextran sulfate sodium for 7 d, and the expression of tumor necrosis factor (TNF)- alpha and interleukin (IL)-1beta in the intestinal mucosa were detected by semi-quantitative reverse transcriptional (RT) PCR. The activation of NF-kappaB in the intestinal mucosa was evaluated by electrophoretic mobility shift assay (EMSA).
RESULTS: The expressions of TNF-alpha and IL-1beta were increased in the intestinal mucosa (P=0.009), and the nuclear binding activity of NF-kappaB was also up-regulated after the onset of colitis.
CONCLUSION: Pro-inflammatory cytokines play important roles in the pathogenesis of UC, and may exacerbate the inflammation of the intestinal mocosa and cause apoptosis of the epithelial cells, possibly under the regulation of NF-kappaB activation.
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