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首页> 外文期刊>American Journal of Physiology >Selectivity of cyclooxygenase isoform activity and prostanoid production in normal and diseased Han:SPRD-cy rat kidneys.
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Selectivity of cyclooxygenase isoform activity and prostanoid production in normal and diseased Han:SPRD-cy rat kidneys.

机译：在正常和患病的Han：SPRD-cy大鼠肾脏中，环氧合酶同工型活性和前列腺素生成的选择性。

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Renal prostanoids are important regulators of normal renal function and maintenance of renal homeostasis. In diseased kidneys, renal cylooxygenase (COX) expression and prostanoid formation are altered. With the use of the Han:Sprague-Dawley-cy rat, the aim of this study was to determine the relative contribution of renal COX isoforms (protein, gene expression, and activity) on renal prostanoid production [thromboxane B(2) (TXB(2), stable metabolite of TXA(2)), prostaglandin E(2) (PGE(2)), and 6-keto-prostaglandin F(1alpha) (6-keto-PGF(1alpha), stable metabolite of PGI(2))] in normal and diseased kidneys. In diseased kidneys, COX-1-immunoreactive protein and mRNA levels were higher and COX-2 levels were lower compared with normal kidneys. In contrast, COX activities were higher in diseased compared with normal kidneys for both COX-1 [0.05 +/- 0.02 vs. 0.45 +/- 0.11 ng prostanoids x min(-1) x mg protein(-1) (P < 0.001)] and COX-2 [0.64 +/- 0.10 vs. 2.32 +/- 0.22 ng prostanoids x min(-1).mg protein(-1) (P< 0.001)]. As the relative difference in activity was greater for COX-1, the ratio of COX-1/COX-2 was higher in diseased compared with normal kidneys, although the predominant activity was still due to the COX-2 isoform in both genotypes. Endogenous and steady-state in vitro levels of prostanoids were approximately 2-10 times higher in diseased compared with normal kidneys. The differences between normal and diseased kidney prostanoids were in the order of TXB(2) > 6-keto-PGF(1alpha) > PGE(2), as determined by higher renal prostanoid levels and COX activity ratios of TXB(2)/6-keto-PGF(1alpha), TXB(2)/PGE(2), and 6-keto-PGF(1alpha)/PGE(2). This specificity in both the COX isoform type and for the prostanoids produced has implications for normal and diseased kidneys in treatments involving selective inhibition of COX isoforms.
机译：肾前列腺素是正常肾功能和维持肾脏稳态的重要调节剂。在患病的肾脏中，肾脏环氧合酶（COX）的表达和前列腺素的形成发生了改变。使用Han：Sprague-Dawley-cy大鼠，本研究的目的是确定肾脏COX亚型（蛋白质，基因表达和活性）对肾前列腺素生成[血栓素B（2）（TXB）的相对贡献（2），TXA（2）），前列腺素E（2）（PGE（2））和6-酮-前列腺素F（1alpha）（6-酮-PGF（1alpha），PGI（ 2））]在正常和患病的肾脏中。与正常肾脏相比，在患病肾脏中，COX-1免疫反应蛋白和mRNA水平较高，而COX-2水平较低。相比之下，患病的COX活性均高于正常肾脏，二者均为COX-1 [0.05 +/- 0.02与0.45 +/- 0.11 ng前列腺素x min（-1）x mg蛋白（-1）（P <0.001 ）]和COX-2 [0.64 +/- 0.10对2.32 +/- 0.22 ng前列腺素x min（-1）.mg蛋白质（-1）（P <0.001）]。由于COX-1活性的相对差异更大，因此患病的COX-1 / COX-2的比率高于正常肾脏，尽管两种基因型的主要活性仍归因于COX-2同工型。与正常肾脏相比，患病的前列腺素的内源性和稳态体外水平约高2-10倍。正常和患病的肾脏前列腺素之间的差异依次为TXB（2）> 6-酮-PGF（1alpha）> PGE（2），这取决于较高的肾脏前列腺素水平和TXB（2）/ 6的COX活性比-keto-PGF（1alpha），TXB（2）/ PGE（2）和6-keto-PGF（1alpha）/ PGE（2）。在涉及选择性抑制COX亚型的治疗中，这种对COX亚型和所产生的前列腺素的特异性对正常肾脏和患病肾脏都有影响。

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