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首页> 外文期刊>Life sciences >Renal production of thromboxane and prostaglandins in a rat model of type 2 diabetes.
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Renal production of thromboxane and prostaglandins in a rat model of type 2 diabetes.

机译：在2型糖尿病大鼠模型中肾脏血栓烷和前列腺素的产生。

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In an investigation of the involvement of prostanoids in the pathogenesis of nephropathy in type 2 diabetes, we repeatedly measured the urinary excretion of prostanoids in both diabetic and healthy rats as the rats aged. Seven rats of the Otsuka Long-Evans Tokushima Fatty strain were used as rats with a model of type 2 diabetes and seven rats of the Long-Evans Tokushima Otsuka strain were used as rats without diabetes. Thromboxane (TX) B2 and 6-keto-prostaglandin (PG) F1alpha, the amounts of which reflect renal production of TXA2 and PGI2, respectively, and PGE2 in urine collected in metabolic cages were assayed when rats were 14, 30, 46, and 54 weeks old. Plasma glucose and urinary protein excretion also were measured periodically. The mean plasma glucose concentration of the diabetic rats was higher than that of the healthy rats throughout the study. At 30 weeks and later, urinary protein excretion by the diabetic rats was greater than that of the healthy rats, and it increased with age. Urinary excretion of TXB2 by the diabetic rats was higher than that of the healthy rats at 14 weeks (52.4+/-23.5 vs. 27.0+/-2.6 ng/day; mean +/- SD, P = .015) and the difference continued to the end of the experiment. Urinary excretion of 6-keto-PGF1alpha by the diabetic rats was high at 14 weeks (52.3+/-12.8 vs. 26.9+/-4.6 ng/day; mean +/- SD, P<.001) but decreased with age and was the same as that of the healthy rats at 54 weeks. The urinary excretion of PGE2 by the two groups of rats was not significantly different. These results suggest that altered renal production of TXA2 and PGI2 is involved in the pathogenesis of diabetic nephropathy in rats with type 2 diabetes.
机译：在对前列腺素参与2型糖尿病肾病发病机制的研究中，我们反复测量了糖尿病大鼠和健康大鼠中老年时前列腺素的尿排泄量。使用大冢Long-Evans德岛肥胖型的7只大鼠作为2型糖尿病模型，使用长Evans德岛大冢脂肪株的7只大鼠作为无糖尿病的大鼠。在大鼠分别为14、30、46和14岁时，测定了血栓烷（TX）B2和6-酮-前列腺素（PG）F1alpha的含量（分别反映了代谢笼中收集的尿液中TXA2和PGI2和PGE2的肾脏生成）。 54周大。还定期检测血浆葡萄糖和尿蛋白排泄。在整个研究过程中，糖尿病大鼠的平均血糖浓度均高于健康大鼠。在30周及以后，糖尿病大鼠的尿蛋白排泄量大于健康大鼠，并且随着年龄的增长而增加。在14周时，糖尿病大鼠的TXB2尿排泄量高于健康大鼠（52.4 +/- 23.5 vs. 27.0 +/- 2.6 ng /天;平均值+/- SD，P = .015），且差异继续进行到实验结束。糖尿病大鼠的6-酮-PGF1α尿排泄在14周时较高（52.3 +/- 12.8 vs. 26.9 +/- 4.6 ng /天;平均+/- SD，P <.001），但随着年龄的增长而降低。在54周时与健康大鼠相同。两组大鼠尿液中PGE2的排泄量无明显差异。这些结果表明，TXA2和PGI2肾脏生成的改变与2型糖尿病大鼠糖尿病肾病的发病机理有关。

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