血管生成实验结肠炎封锁作为一种新的治疗方法。

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Danese年代,Sans M,斯宾塞DM,贝克,我捐F,冷藏室ML, de la丛林C,排除R,邵氏德莱文广告,玛扎尔美联社,Fiocchi C

血管生成实验结肠炎封锁作为一种新的治疗方法。

肠道。2007年6月,56 (6):855 - 62。Epub 2006年12月14日。

PubMed ID

17170016 (在PubMed

]

文摘

背景:Neoangiogenesis慢性炎性疾病是一个重要的组成部分。抑制血管生成在炎症动物模型是一种有效的治疗,但尚未进行实验性结肠炎。目的:探讨atn的影响- 161,一种抗血管生成化合物,实验小鼠结肠炎。方法:白介素10-deficient (IL10(- / -)小鼠和野生型小鼠在ultra-barrier设施(UBF)或传统的住房,并用于实验条件。葡聚糖硫酸钠(DSS)治疗急性结肠炎小鼠作为模型。老鼠接受atn - 161或其炒肽atn - 163。粘膜neoangiogenesis和平均血管密度(MVD)被CD31染色评估。疾病活动指数(DAI)决定,和结肠炎的严重程度由组织学得分决定。结肠细胞因子的生产用ELISA,固有层单核细胞增殖的胸苷掺入。结果:MVD在疾病进展的同时增加IL10(- / -)小鼠在传统住房,而不是IL10(- / -)小鼠UBF。 Angiogenesis also occurred in DSS-treated animals. IL10(-/-) mice with established disease treated with ATN-161, but not with ATN-163, showed a significant and progressive decrease in DAI. The histological colitis score was significantly lower in ATN-161-treated mice than in scrambled peptide-treated mice. Inhibition of angiogenesis was confirmed by a significant decrease of MVD in ATN-161-treated mice than in ATN-163-treated mice. No therapeutic effects were observed in the DSS model of colitis. ATN-161 showed no direct immunomodulatory activity in vitro. CONCLUSION: Active angiogenesis occurs in the gut of IL10(-/-) and DSS-treated colitic mice and parallels disease progression. ATN-161 effectively decreases angiogenesis as well as clinical severity and histological inflammation in IL10(-/-) mice but not in the DDS model of inflammatory bowel disease (IBD). The results provide the rational basis for considering anti-angiogenic strategies in the treatment of IBD in humans.

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药物

atn - 161