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一氧化氮合酶抑制对大鼠三硝基苯磺酸诱导的结肠炎症的时间依赖性作用。

Time-dependent actions of nitric oxide synthase inhibition on colonic inflammation induced by trinitrobenzene sulphonic acid in rats.

作者信息

Kiss J, Lamarque D, Delchier J C, Whittle B J

机构信息

CHU Henri Mondor, INSERM U99, Creteil, France.

出版信息

Eur J Pharmacol. 1997 Oct 8;336(2-3):219-24. doi: 10.1016/s0014-2999(97)01246-6.

DOI:10.1016/s0014-2999(97)01246-6
PMID:9384236
Abstract

The time-dependent actions following pretreatment or delayed administration of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) on colonic inflammation and inducible NO synthase activity following the intrarectal administration of trinitrobenzene sulphonic acid (TNBS) were evaluated in the rat. Intracolonic instillation of TNBS (30 mg in 0.25 ml of 50% ethanol) led to macroscopic injury, an increase of mucosal myeloperoxidase activity and the expression of the Ca2+-independent inducible NO synthase over 8 days. The inflammatory response following TNBS reached maximum levels between 12 and 72 h and then it declined until 14 days. Oral administration of L-NAME (25 mg/kg per 24 h in the drinking water) 2 days before TNBS augmented macroscopic damage and increased colonic inducible NO synthase activity 6, 12, 24 and 72 h after TNBS administration. In contrast, when L-NAME was administered 6 h after TNBS instillation, at time of expression of inducible NO synthase, the macroscopic lesions were reduced, as well as the enhanced inducible NO synthase activity, determined, over 72 h. Delayed (6 h after TNBS) administration of L-NAME also attenuated the colonic myeloperoxidase activity provoked by TNBS, after 24 h. This activity was not affected by pretreatment (2 days before TNBS) with L-NAME. These findings indicate that the timing of administration of non-selective NO synthase inhibitors such as L-NAME, in models of colitis is critical to the eventual outcome. Thus, pretreatment with L-NAME, which will inhibit constitutive NO synthase, exacerbates the subsequent damage following challenge. In contrast, delayed administration of L-NAME at the time of inducible NO synthase expression, has a beneficial action on the colonic injury and inflammation.

摘要

在大鼠中评估了一氧化氮(NO)合酶抑制剂N(G)-硝基-L-精氨酸甲酯(L-NAME)预处理或延迟给药后对直肠内注射三硝基苯磺酸(TNBS)后结肠炎症和诱导型NO合酶活性的时间依赖性作用。结肠内注入TNBS(30 mg溶于0.25 ml 50%乙醇中)导致肉眼可见的损伤、黏膜髓过氧化物酶活性增加以及在8天内钙非依赖性诱导型NO合酶的表达增加。TNBS后的炎症反应在12至72小时之间达到最高水平,然后在14天之前下降。在TNBS给药前2天口服L-NAME(每24小时25 mg/kg溶于饮用水中)会加剧肉眼可见的损伤,并在TNBS给药后6、12、24和72小时增加结肠诱导型NO合酶活性。相反,当在TNBS注入后6小时(即诱导型NO合酶表达时)给予L-NAME,肉眼可见的损伤以及在72小时内测定的增强的诱导型NO合酶活性均降低。L-NAME延迟(TNBS后6小时)给药在24小时后也减弱了TNBS引起的结肠髓过氧化物酶活性。这种活性不受L-NAME预处理(TNBS前2天)的影响。这些发现表明,在结肠炎模型中,非选择性NO合酶抑制剂如L-NAME的给药时间对最终结果至关重要。因此,抑制组成型NO合酶的L-NAME预处理会加剧后续攻击后的损伤。相反,在诱导型NO合酶表达时延迟给予L-NAME对结肠损伤和炎症具有有益作用。

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