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一氧化氮在大鼠黄体溶解过程中对子宫和卵巢前列腺素合成的作用。

Role of nitric oxide on uterine and ovarian prostaglandin synthesis during luteolysis in the rat.

作者信息

Motta A B, Franchi A M, Gimeno M F

机构信息

Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Consejo Nacional de Investigaciones Cientificas y Técnicas (CONICET), Buenos Aires, Argentina.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 1997 Apr;56(4):265-9. doi: 10.1016/s0952-3278(97)90569-x.

DOI:10.1016/s0952-3278(97)90569-x
PMID:9150371
Abstract

In previous studies in our laboratory, we demonstrated that oxytocin (oxy) augmented prostaglandin F(2alpha) (PGF(2alpha)) synthesis via enhancing the uptake of Ca2+ by uterine tissue. On the other hand, we have shown that oxy enhances PGF(2alpha) synthesis in uterine and ovarian tissues during the corpus luteum (CL) regression in the rat. In the present study we explore the possible relation between endogenous nitric oxide (NO) and oxy on PGs synthesis during the luteolytic phase in the rat. The experiments were done in uterine and ovarian preparations isolated from pseudopregnant (psp) rats during the luteolytic phase. Tissues were incubated "in vitro" with 1)- oxy (50 mU/ml), 2)-NMMA (N(G)-monomethyl-L-arginine), a potent NOs inhibitor (300 uM), and 3)- both reagents (oxy + NMMA). NMMA decreases the synthesis of both PGs (PGE and PGF(2alpha)) and oxy enhances PGF(2alpha) synthesis in uterine and ovarian tissue. When reagents were used in combination (oxy + NMMA), we found different results in uterus and ovaries; i.e., in uterine tissue the NO inhibition did not affect the increase of PGF(2alpha) synthesis by oxy. Meanwhile, in ovaries the oxy effect over the PGF(2alpha) synthesis was not seen when NOs was inhibited. Probably oxy acts via different mechanisms on PGF(2alpha) synthesis in uterine and ovarian tissue. This assumption was confirmed when the NOs activity in both tissues (uterine and ovarian) was measured after oxy treatment. We found that oxy enhanced the NOs activity in ovarian tissues from psp rats but did not modify the enzyme activity in uterine tissue.

摘要

在我们实验室之前的研究中,我们证明催产素(oxy)通过增强子宫组织对Ca2+的摄取来增加前列腺素F(2α)(PGF(2α))的合成。另一方面,我们已经表明,在大鼠黄体(CL)退化期间,oxy可增强子宫和卵巢组织中PGF(2α)的合成。在本研究中,我们探讨了大鼠黄体溶解期内源性一氧化氮(NO)与oxy在PGs合成中的可能关系。实验在从假孕(psp)大鼠黄体溶解期分离出的子宫和卵巢制剂中进行。组织在“体外”与1)- oxy(50 mU/ml)、2)- N(G)-单甲基-L-精氨酸(NMMA),一种有效的NO合酶抑制剂(300 μM)和3)- 两种试剂(oxy + NMMA)一起孵育。NMMA可降低两种PGs(PGE和PGF(2α))的合成,而oxy可增强子宫和卵巢组织中PGF(2α)的合成。当联合使用试剂(oxy + NMMA)时,我们在子宫和卵巢中发现了不同的结果;即,在子宫组织中,NO抑制并不影响oxy对PGF(2α)合成的增加。同时,在卵巢中,当NO合酶被抑制时,未观察到oxy对PGF(2α)合成的影响。可能oxy在子宫和卵巢组织中对PGF(2α)合成的作用机制不同。当在oxy处理后测量两种组织(子宫和卵巢)中的NO合酶活性时,这一假设得到了证实。我们发现oxy增强了psp大鼠卵巢组织中的NO合酶活性,但未改变子宫组织中的酶活性。

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