Estimation of mucosal inflammatory mediators in rat DSS-induced colitis -: Possible role of PGE2 in protection against mucosal damage
Estimation of mucosal inflammatory mediators in rat DSS-induced colitis -: Possible role of PGE2 in protection against mucosal damage
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DOI：
10.1159/000051915
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发表时间：
2001-01-01
期刊：
影响因子：
3.2
通讯作者：
Katsu, K
中科院分区：
文献类型：
--
作者：
Hirata, I;Murano, M;Katsu, K
为了探讨UC的黏膜损伤机制，我们制作了葡聚糖硫酸钠（DSS）诱导的大鼠结肠炎模型，检测了DSS结肠炎黏膜的病理学改变、MPO活性、PGE（2）水平以及局部IL-1 β、TNF-α、GRO/CINC-1和IL-10的mRNA表达和分泌。我们估计了粘膜损伤的严重程度与这些局部炎症介质值的变化之间的相关性。神经元浸润明显，MPO活性局部增加，与粘膜损伤的严重程度成比例。IL-1 β、GRO/CINC-1和IL-10的mRNA表达和分泌增加。特别是IL-1 β和GRO/CINC-1的分泌与粘膜损伤的严重程度成比例地增加。然而，TNF-α在结肠炎粘膜中没有增加。从我们的TNF-α数据可以预测异常的巨噬细胞功能和产生不同细胞因子的巨噬细胞亚型的存在。在内源性PGE水平较高的结肠粘膜中，病变不太严重（2），而在内源性PGE水平较低的结肠粘膜中，病变更严重（2），暗示这种化合物是受影响粘膜中炎症发展的抑制因子。提示PGE（2）对UC有一定的治疗价值。版权所有（C）2001 S. Karger AG，巴塞尔。
In order to investigate the mucosal injury mechanism in UC, we made dextran sulfate sodium (DSS)-induced colitis in rat and examined pathological findings, MPO activity, PGE(2) level, and local mRNA expression and secretion of IL-1 beta, TNF-alpha, GRO/CINC-1 and IL-10 in DSS colitis mucosa, Moreover, we estimated the correlation between the severity of mucosal damage and changes of these local inflammatory mediators' values. Neutrophil infiltration was marked and MPO activity was locally increased in proportion to the severity of mucosal damage. The mRNA expression and secretion of IL-1 beta, GRO/CINC-1 and IL-10 were increased. Especially, the secretions of IL-1 beta and GRO/CINC-1 were increased in proportion to the severity of mucosal damage. However, those of TNF-alpha were not increased in the colitis mucosa. An abnormal macrophage function and the presence of macrophage subtypes producing different cytokines would be predicted from our TNF-alpha data. The lesion was less severe in the colonic mucosa with higher levels of endogenous PGE(2), while it was more severe in the colonic mucosa with lower levels of endogenous PGE(2), implicating this compound as an inhibitory factor against the development of inflammation in the affected mucosa. Our results suggest that PGE(2) mig ht have therapeutic applicability to UC. Copyright (C) 2001 S. Karger AG, Basel.