Goodman M J, Kent P W, Truelove S C
Arch Int Pharmacodyn Ther. 1977 Mar;226(1):4-10.
The in vitro inhibition of the glucosamine synthetase activity of rat gastric mucosal homogenates by sodium salicylate and phenylbutazone has been previously reported and has been adduced as a possible mechanism for the ulcerogenic effect of these drugs. This inhibition has been confirmed in human gastric and colonic mucosal homogenates and it is also shown by acetylsalicylic acid and by hydrocortisone hemisuccinate. However, paracetamol and gentamicin, neither of which is known to be ulcerogenic, also inhibited the enzyme to a similar degree to the ulcergenic drugs. This refutes glucosamine synthetase inhibition as the mechanism of the ulcerogenic action of anti-inflammatory drugs.
先前已有报道称，水杨酸钠和保泰松对大鼠胃黏膜匀浆中的氨基葡萄糖合成酶活性具有体外抑制作用，并且这种抑制作用被认为是这些药物产生致溃疡作用的一种可能机制。这种抑制作用在人胃和结肠黏膜匀浆中得到了证实，乙酰水杨酸和氢化可的松半琥珀酸钠也表现出这种抑制作用。然而，对乙酰氨基酚和庆大霉素，二者均不具有致溃疡作用，但它们对该酶的抑制程度与致溃疡药物相似。这就反驳了氨基葡萄糖合成酶抑制是抗炎药物致溃疡作用机制的观点。
