Goto H, Nakazawa S, Ozawa T
Biochem Int. 1987 Feb;14(2):311-7.
We have observed that the contents of prostaglandin (PG) D2 and 6-keto-PGF1 alpha were five times higher than those of PGE2 and PGF2 alpha in rat gastric mucosa. In order to elucidate the role of PGs in the function of gastric mucosa, we studied the effect of hypoxia on the levels of PGs in relation to the degree of gastric mucosal lesions. 6-Keto-PGF1 alpha levels were significantly decreased only by severe and long-term hypoxia (10% O2, 18 hours) when severe ulcerative lesions were observed. PGE2 levels were significantly decreased even by mild and short-term hypoxia (13% O2, 4 hours) when slight ulcerative lesions were observed. PGF2 alpha and PGD2 levels were significantly decreased by mild and short-term hypoxia; however, there was no significant difference from the control group under severe and long-term hypoxia. These results suggest that each of the PGs plays a different role in the pathogenesis of acute gastric mucosal lesions induced by hypoxia.
我们观察到,大鼠胃黏膜中前列腺素(PG)D2和6-酮-PGF1α的含量比PGE2和PGF2α高五倍。为了阐明前列腺素在胃黏膜功能中的作用,我们研究了缺氧对前列腺素水平的影响以及与胃黏膜损伤程度的关系。仅在观察到严重溃疡性病变的严重长期缺氧(10%氧气,18小时)时,6-酮-PGF1α水平才显著降低。在观察到轻微溃疡性病变的轻度短期缺氧(13%氧气,4小时)时,PGE2水平也显著降低。PGF2α和PGD2水平在轻度短期缺氧时显著降低;然而,在严重长期缺氧时与对照组无显著差异。这些结果表明,每种前列腺素在缺氧诱导的急性胃黏膜病变的发病机制中发挥不同作用。