的interleukin-1 beta-converting酶抑制剂pralnacasan降低硫酸葡聚糖sodium-induced小鼠结肠炎和辅助T 1 T细胞活化。

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loh F,鲍尔C,蓝道N, Schmall K, Siegmund B,莱尔哈,多尔M, Schoenharting M, Endres年代,Eigler

的interleukin-1 beta-converting酶抑制剂pralnacasan降低硫酸葡聚糖sodium-induced小鼠结肠炎和辅助T 1 T细胞活化。

J Exp其他杂志》2004年2月,308 (2):583 - 90。Epub 2003 11月10。

PubMed ID

14610233 (在PubMed

]

文摘

促炎细胞因子白细胞介素(IL) 1β和地震应该发挥着至关重要的作用在人类炎症性肠病的发病机制。发挥生物活性的前体IL-1beta和地震-需要由interleukin-1beta-converting裂解酶(冰)。地震诱发的合成IFN-gamma T细胞和NK细胞。在目前的研究中,我们调查的影响具体冰抑制剂pralnacasan硫酸葡聚糖sodium-induced小鼠结肠炎。结肠炎在BALB / c小鼠诱导3.5%硫酸葡聚糖钠溶解在饮用水了10天。Pralnacasan每天口服或腹腔内接种。评估体内疗效,临床疾病活动指数为每天进行评估。结肠长度、表达的地震在结肠组织移行细胞的表达(IFN-gamma) paraaortal淋巴细胞,并系统分析了在脾细胞生产IFN-gamma验尸。腹腔内注射pralnacasan显著降低临床评分与葡聚糖硫酸酯钠相比对照组每天6到10天。口服的pralnacasan临床评分也显著减少了天8和9。 Administration of pralnacasan i.p. reduced the expression of intracolonic IL-18 significantly. Furthermore, pralnacasan reduced the number of IFN-gamma-positive lymphocytes in paraaortal lymph nodes. IFN-gamma synthesis in stimulated splenocytes was significantly suppressed in all pralnacasan-treated groups. No side effects of pralnacasan were observed. In conclusion, pralnacasan is effective in the prevention of dextran sulfate sodium-induced colitis. This effect is probably mediated by suppression of the proinflammatory cytokines IL-18, IL-1beta, and IFN-gamma.

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药物

Pralnacasan