Production of 6-oxo-prostaglandin F1 alpha and prostaglandin E2 by isolated glomeruli from normal and diabetic rats.
Production of 6-oxo-prostaglandin F1 alpha and prostaglandin E2 by isolated glomeruli from normal and diabetic rats.
复制标题
正常和糖尿病大鼠的分离肾小球产生 6-氧代前列腺素 F1 α 和前列腺素 E2。
DOI：
10.1136/bmj.284.6324.1215
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
R. Larkins
中科院分区：
文献类型：
--
作者：
S. Rogers;R. Larkins
用放射免疫分析法测定链脲佐菌素诱导的糖尿病大鼠和非糖尿病大鼠离体肾小球上清液中6-氧代-前列腺素F1 α（6-oxo-PGF 1 α）和前列腺素E2（PGE 2）的产生。同时测量这些大鼠的椎间盘6-oxo-PGF 1 α的产生。如前所示，糖尿病大鼠的主动脉盘产生的6-氧代-PGF 1 α显著低于非糖尿病大鼠的主动脉盘（糖尿病大鼠为1.99 +/- SEM 0.27 ng，非糖尿病大鼠为2.92 +/- 0.46 ng/mg主动脉净重; p <0.05）。相比之下，糖尿病大鼠的离体肾小球产生的6-oxo-PGF 1 α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）。类似地，PGE 2的产生在糖尿病肾小球中没有减少（糖尿病1.20 +/-0.15ng对非糖尿病0.91 +/-0.12ng/微克肾小球DNA）。得出的结论是，实验性糖尿病中前列环素和6-氧代-PGF 1 α的产生存在地区差异。前列环素产生减少可能导致糖尿病患者对动脉粥样硬化的易感性增加，但不太可能在微血管病的发病机制中发挥作用。
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.