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Mucosal damage induced by preferential COX-1 and COX-2 inhibitors: Role of prostaglandins and inflammatory response

机译：优先COX-1和COX-2抑制剂引起的粘膜损伤：前列腺素的作用和炎症反应

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Nonsteroidal anti-inflammatory drugs (NSAID) are well known to induce gastric mucosal damage including bleeding, ulceration and perforation in humans and animals too. These effects are related with the inhibition of the enzyme cyclooxygenase, which is the main established mechanism of action for these drugs. Fasted rats were given piroxicam, preferential COX-1 inhibitor (10-20 mg/kg) or meloxicam, preferential COX-2 inhibitor (7.5-15 mg/kg) orally. Six or nine hours (h) later, respectively, the stomach was excised, the severity of the damage assessed and myeloperoxidase (MPO) activity measured, as well as prostaglandin PGE(2) content. Furthermore, in order to assess the effects of these oxicams over previously damaged gastric mucosa, 1 ml of 0.6 N HCl was administered p.o. followed, 1 h after, of the correspondent dose of each NSAID, and the same parameters were determined. Oral administration of both drugs dose-dependently caused acute gastric haemorrhage erosions. Myeloperoxidase activity was significantly increased by piroxicam administration. In addition, PGE(2) content was significantly reduced. The association between the administration of the acid and NSAID caused a worsening of the damage and, while myeloperoxidase activity did not modify by both piroxicam and meloxicam, PGE(2) levels were reduced. These results suggest that the PG derived from both COX-1 and COX-2 pathway plays a beneficial role in the gastroprotection, and thus caution should be exercise in the clinical use of preferential COX-2 inhibitors. (C) 2003 Elsevier Inc. All rights reserved. [References: 48]
机译：众所周知，非甾体抗炎药（NSAID）也会诱发人和动物的胃粘膜损害，包括出血，溃疡和穿孔。这些作用与环氧合酶的抑制有关，环氧合酶是这些药物的主要作用机理。禁食的大鼠口服给予吡罗昔康，优先COX-1抑制剂（10-20 mg / kg）或美洛昔康，优先COX-2抑制剂（7.5-15 mg / kg）。分别在六小时或九小时（h）后切除了胃，评估了损伤的严重程度，并测量了髓过氧化物酶（MPO）活性，以及​​前列腺素PGE（2）的含量。此外，为了评估这些抗氧化剂对先前受损的胃粘膜的作用，可口服1 ml 0.6 N HCl。随后，在每剂非甾体抗炎药的相应剂量1小时后，确定相同的参数。两种药物的口服剂量依赖性地引起急性胃出血侵蚀。吡罗昔康给药显着增加了髓过氧化物酶活性。此外，PGE（2）含量显着降低。酸和NSAID的给药之间的联系导致损害加剧，尽管吡罗昔康和美洛昔康均未改变髓过氧化物酶的活性，但PGE（2）水平降低了。这些结果表明，源自COX-1和COX-2途径的PG在胃保护中起有益作用，因此在临床上优先使用COX-2抑制剂时应谨慎行事。 （C）2003 Elsevier Inc.保留所有权利。 [参考：48]

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