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大鼠实验性结肠炎的炎症介质

Inflammatory mediators of experimental colitis in rats.

作者信息

Rachmilewitz D, Simon P L, Schwartz L W, Griswold D E, Fondacaro J D, Wasserman M A

机构信息

Department of Pharmacology, Smith Kline and French Laboratories, King of Prussia, Pennsylvania.

出版信息

Gastroenterology. 1989 Aug;97(2):326-37. doi: 10.1016/0016-5085(89)90068-1.

DOI:10.1016/0016-5085(89)90068-1
PMID:2545504
Abstract

Colonic inflammation was induced in rats by intracolonic administration of 0.25 ml of 50% ethanol containing 30 mg of trinitrobenzene sulfonic acid (TNB). Control rats were treated with 0.25 ml of 50% ethanol or with 30 mg of TNB in 0.25 ml of saline. After 24 h, mucosal ulceration and hemorrhage were observed in TNB/ethanol-, 50% ethanol-, and to a lesser extent, in TNB/saline-treated rats. After 1 wk, mucosal damage was completely resolved in the 50% ethanol and TNB/saline-treated rats but the lesions in the TNB/ethanol-treated rats persisted and progressed to a chronic active inflammatory process after 3 wk. Myeloperoxidase activity was significantly elevated in mucosal scrapings from all treatment groups at all time intervals when macroscopic and microscopic mucosal injury was evident. Interleukin-1 was found to be the most sensitive indicator of mucosal inflammation, and its mucosal values correlated with myeloperoxidase activity. Leukotriene B4 was increased in control rats at 1 wk and in TNB/ethanol-treated rats at all time intervals. The maximal increase in leukotriene B4 was observed at 1 wk. Thromboxane B2 generation was reduced while platelet activating factor generation was not increased in TNB/ethanol-treated rats. These results indicate that in this TNB/ethanol model of gut inflammation, myeloperoxidase activity and interleukin-1 are reliable and sensitive indicators of colonic inflammation, and that thromboxane B2 is not involved in the acute lesions, whereas leukotriene B4 appears in the chronic active inflammatory response.

摘要

通过向大鼠结肠内注射0.25 ml含30 mg三硝基苯磺酸(TNB)的50%乙醇诱导结肠炎症。对照大鼠接受0.25 ml 50%乙醇或0.25 ml盐水中含30 mg TNB的处理。24小时后,在TNB/乙醇处理组、50%乙醇处理组以及程度较轻的TNB/盐水处理组大鼠中观察到黏膜溃疡和出血。1周后,50%乙醇和TNB/盐水处理组大鼠的黏膜损伤完全消退,但TNB/乙醇处理组大鼠的损伤持续存在,并在3周后进展为慢性活动性炎症过程。在所有时间点,当肉眼和显微镜下可见黏膜损伤时,所有处理组的黏膜刮片中髓过氧化物酶活性均显著升高。白细胞介素-1被发现是黏膜炎症最敏感的指标,其黏膜值与髓过氧化物酶活性相关。白三烯B4在对照大鼠1周时升高,在TNB/乙醇处理组大鼠的所有时间点均升高。白三烯B4的最大升高在1周时观察到。TNB/乙醇处理组大鼠中血栓素B2生成减少,而血小板活化因子生成未增加。这些结果表明,在这种TNB/乙醇诱导的肠道炎症模型中,髓过氧化物酶活性和白细胞介素-1是结肠炎症可靠且敏感的指标,血栓素B2不参与急性病变,而白三烯B4出现在慢性活动性炎症反应中。

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Inflammatory mediators of experimental colitis in rats.大鼠实验性结肠炎的炎症介质
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Treatment with 16,16'-dimethyl prostaglandin E2 before and after induction of colitis with trinitrobenzenesulfonic acid in rats decreases inflammation.在大鼠中,用三硝基苯磺酸诱导结肠炎前后给予16,16'-二甲基前列腺素E2进行治疗可减轻炎症。
Gastroenterology. 1989 May;96(5 Pt 1):1290-300. doi: 10.1016/s0016-5085(89)80016-2.

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