Rogers S P, Larkins R G
Br Med J (Clin Res Ed). 1982 Apr 24;284(6324):1215-7. doi: 10.1136/bmj.284.6324.1215.
Production of 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) and prostaglandin E2 (PGE2) was measured by radioimmunoassay in supernatants of isolated glomeruli from rats with streptozocin-induced diabetes and non-diabetic rats. Production of 6-oxo-PGF1 alpha by discs of aortas from these rats was measured at the same time. As shown before, aortic discs from diabetic rats produced significantly less 6-oxo-PGF1 alpha than aortic discs from non-diabetic rats (diabetic 1.99 +/- SEM 0.27 ng v non-diabetic 2.92 +/- 0.46 ng/mg net weight aorta; p less than 0.05). In contrast production of 6-oxo-PGF1 alpha by isolated glomeruli was not reduced in the diabetic rats (diabetic 77 +/- 7 pg v non-diabetic 70 +/- 8 pg/micrograms glomerular DNA). Similarly production of PGE2 was not diminished in the diabetic glomeruli (diabetic 1.20 +/- 0.15 ng v non-diabetic 0.91 +/- 0.12 ng/microgram glomerular DNA). It is concluded that regional differences in production of prostacyclin and 6-oxo-PGF1 alpha occur in experimental diabetes. Diminished prostacyclin production may contribute to the increased susceptibility of diabetic patients to atherosclerosis but is less likely to have a role in the pathogenesis of microangiopathy.
采用放射免疫分析法测定链脲佐菌素诱导糖尿病大鼠和非糖尿病大鼠分离肾小球上清液中6-氧代前列腺素F1α(6-oxo-PGF1α)和前列腺素E2(PGE2)的生成量。同时测定这些大鼠主动脉片生成6-氧代-PGF1α的量。如前所示,糖尿病大鼠的主动脉片生成的6-氧代-PGF1α明显少于非糖尿病大鼠(糖尿病大鼠为1.99±标准误0.27 ng,非糖尿病大鼠为2.92±0.46 ng/毫克主动脉净重;p<0.05)。相比之下,糖尿病大鼠分离肾小球生成6-氧代-PGF1α的量并未减少(糖尿病大鼠为77±7 pg,非糖尿病大鼠为70±8 pg/微克肾小球DNA)。同样,糖尿病肾小球中PGE2的生成也未减少(糖尿病大鼠为1.20±0.15 ng,非糖尿病大鼠为0.91±0.12 ng/微克肾小球DNA)。结论是,实验性糖尿病中前列环素和6-氧代-PGF1α的生成存在区域差异。前列环素生成减少可能导致糖尿病患者动脉粥样硬化易感性增加,但在微血管病变发病机制中作用较小。