首页> 外文期刊>The Journal of Reproduction and Development >Luteoprotective mechanisms of prostaglandin F2 alpha stimulated by luteinizing hormone in the bovine corpus luteum.
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Luteoprotective mechanisms of prostaglandin F2 alpha stimulated by luteinizing hormone in the bovine corpus luteum.

机译:黄体生成素在黄体中刺激激素对前列腺素F2α的保护作用。

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摘要

Luteinizing hormone (LH) regulates several ovarian functions. However, the luteoprotective mechanisms of LH involved in the maintenance of bovine corpus luteum (CL) function are not well understood. Since prostaglandin F2 alpha (PGF), PGE2 and progesterone (P4) are well documented as antiapoptotic factors in the bovine CL, we hypothesized that LH protects the CL by stimulating the local production and action of PGF, PGE2 and P4. Cultured bovine luteal cells obtained at the mid-luteal stage (days 8-12 of the estrous cycle) were treated with LH (10 ng/ml), onapristone (OP: a specific P4 receptor antagonist, 100 micro M) and indomethacin [INDO; a cyclooxygenase (COX) inhibitor, 100 micro M] for 24 h. LH with and without OP significantly increased the mRNA and protein expressions of COX-2, PGF synthase and carbonyl reductase (P<0.05) but not the mRNA and protein expressions of COX-1 and PGE synthase in bovine luteal cells. In addition, these treatments significantly increased PGF and P4 production (P<0.05) but not PGE2 production. Luteal cell viability was significantly increased by LH alone (P<0.05), but LH-increased cell viability was reduced by LH in combination with INDO as well as OP (P<0.05). The overall results suggest that LH prevents luteal cell death by stimulating luteal PGF and P4 production and supports CL function during the luteal phase in cattle.
机译:黄体生成素(LH)调节几种卵巢功能。但是,LH的黄体保护机制涉及牛黄体(CL)功能的维持尚不十分清楚。由于前列腺素F2 alpha(PGF),PGE2和孕酮(P4)作为牛CL中的抗凋亡因子已有很好的文献报道,我们假设LH通过刺激PGF,PGE2和P4的局部产生和作用来保护CL。在黄体中期(发情周期的第8-12天)获得的培养的黄体黄体细胞用LH(10 ng / ml),onapristone(OP:一种特定的P4受体拮抗剂,100 micro M)和消炎痛[INDO]处理。 ;环氧化酶(COX)抑制剂100 microM]持续24小时。有和没有OP的LH显着增加牛黄体细胞中COX-2,PGF合酶和羰基还原酶的mRNA和蛋白质表达(P <0.05),但不增加COX-1和PGE合酶的mRNA和蛋白质表达。另外,这些治疗显着增加了PGF和P4的产生(P <0.05),但没有增加PGE 2的产生。单独使用LH可使黄体细胞活力显着提高(P <0.05),但与INDO和OP联合使用LH可使LH增加的细胞活力降低(P <0.05)。总体结果表明,LH通过刺激黄体的PGF和P4生成来预防黄体细胞死亡,并在牛的黄体期支持CL功能。

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