Araujo Reno R, Ginther O J, Ferreira Jair C, Palhão Miller M, Beg Mohd A, Wiltbank Milo C
Department of Dairy Science, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.
Biol Reprod. 2009 Aug;81(2):426-37. doi: 10.1095/biolreprod.108.073825. Epub 2009 Mar 4.
The hypothesis was tested that estradiol (E2) from the ovarian follicles controls time of luteolysis. Time of luteolysis was evaluated by multiple measures of corpus luteum (CL) structure (area, volume) and function (progesterone [P4], luteal blood flow). The hypothesis for experiment 1 was that repeated ablation of follicles would reduce circulating E2 and delay luteolysis. Heifers were randomly assigned on Day 9 (Day 0 = ovulation) to three groups. All follicles >or=4 mm were ablated on Day 9 (group FA9; n = 6); Days 9-15 (group FA15; n = 6); or Days 9-21 (group FA21; n = 7). As expected, follicular ablation delayed (P < 0.001) the rise in circulating E2 and peak E2 concentrations (FA9, Day 17.6 +/- 0.7; FA15, Day 20.3 +/- 0.3; FA21, Day 24.9 +/- 0.3). Luteolysis (based on each measure) was delayed (P < 0.005) by repeated ablation of follicles, with earlier luteolysis (based on P4 decrease) in FA9 (Day 15.2 +/- 0.8) than FA15 (Day 16.5 +/- 0.4), and a further delay in FA21 (Day 18.3 +/- 0.5). The hypothesis of experiment 2 was that exogenous treatment with E2 would stimulate prostaglandin F(2alpha) (PGF) secretion and prevent the delay in luteolysis associated with follicular ablations. Follicles >or=4 mm were ablated from Day 9 to Day 17 (n = 15). Heifers were treated on Days 13 and 15 with 1.0 mg of estradiol benzoate (FAE2; n = 7) or vehicle (FAV; n = 8). Treatment with E2 induced PGF secretion (detected by PGF metabolite) and induced earlier (P < 0.02) luteolysis in FAE2 than in FAV, whether determined by circulating P4 or by area, volume, or blood flow of CL. In summary, ablation of follicles (>or=4 mm) delayed and treatment with E2 hastened luteolysis in heifers with ablated follicles. Thus, these results are consistent with an essential role for follicle E2 in timing of luteolysis.
研究人员对卵巢卵泡分泌的雌二醇（E2）控制黄体溶解时间这一假说进行了验证。通过对黄体（CL）的结构（面积、体积）和功能（孕酮[P4]、黄体血流量）进行多项测量来评估黄体溶解时间。实验1的假说是，反复破坏卵泡会降低循环中的E2水平并延迟黄体溶解。在第9天（第0天=排卵）将小母牛随机分为三组。在第9天对所有直径≥4mm的卵泡进行破坏（FA9组；n = 6）；在第9 - 15天（FA15组；n = 6）；或在第9 - 21天（FA21组；n = 7）。正如预期的那样，卵泡破坏延迟了（P < 0.001）循环中E2的升高和E2峰值浓度（FA9组，第17.6±0.7天；FA15组，第20.3±0.3天；FA21组，第24.9±0.3天）。反复破坏卵泡会延迟（P < 0.005）黄体溶解（基于各项测量指标），FA9组（基于P4降低，第15.2±0.8天）的黄体溶解比FA15组（第16.5±0.4天）更早，而FA21组则进一步延迟（第18.3±0.5天）。实验2的假说是，外源性给予E2会刺激前列腺素F2α（PGF）分泌，并防止与卵泡破坏相关的黄体溶解延迟。从第9天到第17天破坏直径≥4mm的卵泡（n = 15）。在第13天和第15天给小母牛注射1.0mg苯甲酸雌二醇（FAE2组；n = 7）或赋形剂（FAV组；n = 8）。给予E2治疗可诱导PGF分泌（通过PGF代谢产物检测），并且无论通过循环中的P4还是通过CL的面积、体积或血流量来确定，FAE2组的黄体溶解都比FAV组更早（P < 0.02）。总之，破坏卵泡（直径≥4mm）会延迟黄体溶解，而给予E2治疗会加速卵泡被破坏的小母牛的黄体溶解。因此，这些结果与卵泡E2在黄体溶解时间方面的重要作用是一致的。
