No evidence for an involvement of the p38 and JNK mitogen-activated protein in inflammatory bowel diseases
No evidence for an involvement of the p38 and JNK mitogen-activated protein in inflammatory bowel diseases
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DOI：
10.1007/s10620-006-9116-2
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发表时间：
2006-08-01
影响因子：
3.1
通讯作者：
Desreumaux, Pierre
中科院分区：
文献类型：
--
作者：
Malamut, Georgia;Cabane, Candice;Desreumaux, Pierre
丝裂原活化蛋白（MAPK）在炎症性肠病（IBD）中的作用仍然是一个谜。我们试图评估p38和JNK MAPK在IBD和2,4,6-三硝基苯磺酸（TNBS）诱导的结肠炎中的表达和活性；以及p38抑制剂SB203580在TNBS结肠炎中的作用。测定了28例IBD患者和19例对照组以及77例TNBS或对照组小鼠结肠黏膜中p38和JNK的含量。结肠炎的严重程度通过生存、宏观和微观评分以及分子标记来评估。IBD患者和对照组中p38和JNK的表达和活性相似，不受炎症的影响。在小鼠中，p38和JNK的表达或活性在结肠炎诱导后没有增加。SB203580降低p38活性，但无临床和生物学治疗效果。总之，这些结果最小化了p38和JNK在炎症性结肠炎中的作用，以及p38作为IBD治疗靶点的兴趣。
Involvement of mitogen-activated protein (MAPK) in inflammatory bowel disease (IBD) remains enigmatic. We sought to evaluate the expression and activity of p38 and JNK MAPK in IBD and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis; and the effects of a p38 inhibitor, SB203580, in TNBS colitis. P 38 and JNK were quantified in colonic mucosa of 28 IBD patients and 19 controls and in 77 TNBS or control mice treated or not with SB203580. Colitis severity was assessed by survival, macroscopic and microscopic scoring, and molecular markers. Expression and activity of p38 and JNK were similar in IBD patients and controls and not modified by inflammation. In mice, p38 and JNK expression or activity did not increase following the induction of colitis. SB203580 decreased the p38 activity but displayed no clinical nor biological therapeutic effect. In conclusion, these results minimize the role of p38 and JNK in inflammatory colitis and the interest of p38 as a therapeutic target in IBD.