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PPARγ pathway in the treatment of ulcerative colitis TMP 's role

Author: HeXiangYi
Tutor: ChenWeiXiong;ZhuJinShui;ChenNiWei;ChenJinLian
School: Shanghai Jiaotong University
Course: Internal Medicine
Keywords: TMP Ulcerative colitis Peroxisome proliferator-activated receptor -γ Nuclear factor -κB Mitogen-activated protein kinase
CLC: R285.5
Type: Master's thesis
Year: 2008
Downloads: 172
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Background and purpose of the colonic mucosa of ulcerative colitis is a chronic non-specific inflammation of unknown etiology, prolonged course, often recurrent, the current lack of effective treatment methods. Studies show that ligustrazine on ulcerative colitis have a therapeutic effect, but the mechanism is unknown. Peroxisome proliferator-activated receptors (peroxisome proliferators-activated receptor, PPAR) are a class of ligand-activated nuclear transcription factor superfamily. More evidence that PPARγ involved the development of ulcerative colitis. This study aimed to investigate the PPARγ pathway in the TMP treatment of ulcerative colitis in rats. Methods oxazolone-induced mice as a model of ulcerative colitis were randomly divided into normal control group (NC), ulcerative colitis saline group (OXZ group), ulcerative colitis group given TMP (TMP group), given PPARγ antagonist BADGE ulcerative colitis group (BA group), and while giving the TMP and BADGE ulcerative colitis group (TMP BA group). Evaluation of inflammation observed in each group (DAI, gross and histologic injury score, MPO values); using quantitative PCR method to detect the intestinal PPARγ, nuclear factor-κB (NF-κB) p65, iNOS, COX-2, tumor necrosis factor α (TNF-α) mRNA expression; immunohistochemical assay PPARγ, NF-κB p65 protein. Western blot detection of phosphorylated p38 MAPK (p-p38 MAPK) protein. Results Compared with NC group, OXZ inflammatory evaluation group were significantly higher (P lt; 0.01), PPARγmRNA and protein decreased significantly (P lt; 0.01), NF-κB p65 and TNF-α expression were significantly higher ( P lt; 0.01). After application of TMP, UC inflammation evaluation group was significantly lower than those OXZ (P lt; 0.01), PPARγmRNA and protein expression increased (P lt; 0.01), NF-κB p65 and TNF-α expression were decreased ( P lt; 0.01). Immunohistochemistry showed that BA group PPARγ negative, compared with the BA group OXZ evaluation of inflammation, NF-κB p65, p-p38 MAPK protein were increased (P lt; 0.05). TMP BA and BA group compared Immunohistochemistry showed that PPARγ positive rate was significantly increased inflammation evaluation, NF-κB p65, p-p38 MAPK protein were decreased (P lt; 0.01). Conclusion PPARγ down in the UC model mice, blocking PPARγ make intestinal inflammation, ulcerative colitis worse. Showed that PPARγ pathway is involved in the development of ulcerative colitis. TMP alter the expression of PPARγ and reverse blocking PPARγ deterioration caused by ulcerative colitis, suggesting that the role of TMP treatment of ulcerative colitis and PPARγ pathway, but not dependent on PPARγ.

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