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首页> 外文期刊>Free radical research >Effects of oxicam inhibitors of cyclooxygenase on oxidative stress generation in rat gastric mucosa. A comparative study.
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Effects of oxicam inhibitors of cyclooxygenase on oxidative stress generation in rat gastric mucosa. A comparative study.

机译：环氧加氧酶抑制剂对大鼠胃粘膜氧化应激的影响。一项比较研究。

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摘要

The aim of this study was to compare the effects of two nonsteroidal anti-inflammatory drugs (NSAID), members of the same family with a different cyclooxygenase (COX) inhibition selectivity, meloxicam, preferent COX-2 inhibitor, and piroxicam, preferent COX-1 inhibitor, on oxygen radical generation in rat gastric mucosa. Therefore, the activity of oxidative stress-related enzymes such as xanthine oxidase (XO), superoxide dismutase (SOD) and glutathione (GSH) homeostasis were studied in rats. Gastric prostaglandins (PG) were also assessed as a measure of COX-1 inhibition. Both oxicams produced a similar extent of the gastric mucosal damage and a significant decrease in PGE2 synthesis, however only piroxicam induced an increase of both myeloperoxidase (MPO) activity and tumor necrosis factor (TNF)-alpha content in the gastric mucosa, indicating that neutrophil-derived free radicals were involved in gastric injury. Furthermore, both compounds reduced SOD activity and increased XO activity in gastric mucosa. Our results also revealed modifications in GSH metabolism: although glutathione peroxidase (GSH-px) activity was unaffected by meloxicam or piroxicam administration, both glutathione reductase (GSSG-rd) activity and total GSH content were significantly decreased after dosing. These results suggest that under our experimental conditions, meloxicam, preferential COX-2 inhibitor causes rates of gastric lesion in rats comparable to those seen with the traditional NSAID piroxicam, preferential COX-1 inhibitor. In addition to suppression of systemic COX activity, oxygen radicals, probably derived via the XO, and neutrophils play an important role in the production of damage induced by both oxicams. Moreover, the decrease in SOD activity and changes in glutathione homeostasis in gastric mucosa may also contribute to pathogenesis of meloxicam- or piroxicam-induced gastropathy.
机译：这项研究的目的是比较两种非甾体类抗炎药（NSAID）的作用，它们是具有不同环加氧酶（COX）抑制选择性的同一家族成员，美洛昔康（首选COX-2抑制剂）和吡罗昔康（首选COX- 1种抑制剂，对大鼠胃粘膜中氧自由基的产生。因此，在大鼠中研究了氧化应激相关酶的活性，如黄嘌呤氧化酶（XO），超氧化物歧化酶（SOD）和谷胱甘肽（GSH）稳态。胃前列腺素（PG）也被评估为COX-1抑制的量度。两种抗氧化剂都产生相似程度的胃粘膜损害，并显着降低PGE2合成，但是只有吡罗昔康诱导胃粘膜中的髓过氧化物酶（MPO）活性和肿瘤坏死因子（TNF）-α含量均增加，表明嗜中性白细胞自由基参与胃损伤。此外，两种化合物均降低了胃粘膜中的SOD活性并增加了XO活性。我们的研究结果还揭示了GSH代谢的改变：尽管服用美洛昔康或吡罗昔康不影响谷胱甘肽过氧化物酶（GSH-px）活性，但给药后谷胱甘肽还原酶（GSSG-rd）活性和总GSH含量均显着降低。这些结果表明，在我们的实验条件下，美洛昔康（首选COX-2抑制剂）引起的大鼠胃部病变的发生率与传统NSAID吡罗昔康（首选COX-1抑制剂）所观察到的相当。除了抑制全身性COX活性外，可能通过XO衍生的氧自由基和中性粒细胞在产生两种氧嘧啶引起的损伤中也起着重要作用。此外，胃黏膜中SOD活性的降低和谷胱甘肽稳态的变化也可能是美洛昔康或吡罗昔康诱发的胃病的发病机理。

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