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首页> 外文期刊>Inflammation >Different Mechanisms in Formation and Prevention of Indomethacin-induced Gastric Ulcers
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Different Mechanisms in Formation and Prevention of Indomethacin-induced Gastric Ulcers

机译：消炎痛诱发胃溃疡形成和预防的不同机制

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Indomethacin is an indol derivative, non-steroidal, anti-inflammatory drug with anti-inflammatory, analgesic, and antipyretic effects. Indomethacin became the first-choice drug to produce an experimental ulcer model as a result of having a higher ulcerogenic potential than other non-steroidal anti-inflammatory drugs (NSAIDs). There have been several conflicting reports about the ulcerogenic mechanism of indomethacin; the mechanism is still unclear. It has been suggested that indomethacin induces gastric damage via inhibiting the release of protective factors like cyclooxygenase-1 (COX-1), prostaglandin E2 (PGE2), bicarbonate, and mucus; increasing aggressive factors like acid; and increasing oxidant parameters while decreasing antioxidant parameters. Classic antiulcer drugs are known to produce antiulcer effects by activating against indomethacin (increasing PGE2, mucus, and bicarbonate production; inhibiting acid secretion; decreasing oxidant parameters; and increasing antioxidants). However, some antiulcer drugs have been shown to inhibit indomethacin-induced ulcers without affecting acid and mucus secretion or oxidant parameters, as well as to inhibit the production of protective factors like COX-1, PGE2, and bicarbonate, and to reduce antioxidant parameters. In order to resolve the contradictions in the abovementioned data, this review hypothesized a relationship between indomethacin-induced ulcers and α 2 adrenergic receptors. It is suggested that blockage of α 2 adrenergic receptors may be responsible for the increase in the aggressive factors induced by indomethacin, and stimulation of α 2 adrenergic receptors may be responsible for the increase of protective factors induced by antiulcer drugs.
机译：消炎痛是吲哚衍生物，非甾体抗炎药，具有消炎，镇痛和解热作用。消炎痛因其比其他非甾体类抗炎药（NSAIDs）具有更高的致溃疡潜力，因此成为产生实验性溃疡模型的首选药物。关于吲哚美辛的致溃疡机理，已有几篇相互矛盾的报道。机制尚不清楚。有人提出消炎痛可通过抑制环氧合酶-1（COX-1），前列腺素E2（PGE2），碳酸氢盐和粘液等保护因子的释放而引起胃损伤。增加攻击性因素，例如酸；并增加氧化剂参数，同时降低抗氧化剂参数。已知经典的抗溃疡药会通过激活消炎痛来产生抗溃疡作用（增加PGE2，粘液和碳酸氢盐的产生；抑制酸的分泌；降低氧化剂的参数；以及增加抗氧化剂）。但是，已显示某些抗溃疡药可抑制消炎痛诱导的溃疡，而不会影响酸和粘液的分泌或氧化剂参数，并抑制诸如COX-1，PGE2和碳酸氢盐等保护因子的产生，并降低抗氧化剂的参数。为了解决上述数据中的矛盾，本评价假设了消炎痛诱发的溃疡与α2肾上腺素能受体之间的关系。提示阻断α2肾上腺素受体可能是消炎痛诱导的攻击性因子增加的原因，刺激α2肾上腺素受体可能是抗溃疡药物诱导的保护因子增加的原因。

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