摘要
瞄准：为了探索 Diammonium 的反煽动性的机制，在 ulcerative 的一个老鼠模型的 Glycyrrhizinate 由乙酸导致了。方法：Spragur-Dawley 雌老鼠被划分成四个组：Diammonium Glycyrrhizinate 组，地塞米松组，乙酸控制和正常控制组。结肠的发炎被疾病活动索引，粗野词法损坏，组织学的损害和结肠的 myeloperoxidase 活动评估。Immunohistochemistry 被用来在结肠的粘膜检测 NF-kappaB， TNF-alpha 和 ICAM-1 的表示。结果：把控制，显示出的两 Diammonium Glycyrrhizinate 和地塞米松比作乙酸重要反煽动性的效果(P 【
0.01 ) 。在结肠的粘膜的 NF-kappaB， TNF-alpha 和 ICAM-1 的表示比在乙酸组在 Diammonium Glycyrrhizinate 组和地塞米松组是显著地更低的。结论：Diammonium Glycyrrhizinate 能在 ulcerative 的一个老鼠模型减少煽动性的损害。这可以在结肠的粘膜经由 NF-kappaB， TNF-alpha 和 ICAM-1 的抑制发生。
AIM： To explore the anti-inflammatory mechanism of Diammonium Glycyrrhizinate in a rat model of ulcerative colitis induced by acetic acid. METHODS： Spragur-Dawley female rats were divided into four groups： Diammonium Glycyrrhizinate group, dexamethasone group, acetic acid control and normal control group. Colonic inflammation was evaluated by disease activity index, gross morphologic damage, histological injury and colonic myeloperoxidase activity. Immunohistochemistry was used to detect the expression of NF-κB, TNF-α and ICAM-1 in colonic mucosa. RESULTS： Compared to the acetic acid control, both Diammonium Glycyrrhizinate and dexamethasone showed a significant anti-inflammatory effect （P 〈 0.01）. The expression of NF-κB, TNF-α and ICAM-1 in colonic mucosa was significantly lower in the Diammonium Glycyrrhizinate group and dexamethasone group than in the acetic acid group. CONCLUSION： Diammonium Glycyrrhizinate could reduce inflammatory injury in a rat model of ulcerative colitis. This may occur via suppression of NF-κB, TNF-αand ICAM-1 in colonic mucosa.
基金
Supported by the Health Ministry of Shandong Province, No. 2005HW147
关键词
抗炎作用
磷酸氢二铵
肠溃疡
治疗
Ulcerative colitis
Diammonium Glycyrrhizinate
Mechanism
