Estradiol inhibits milk production in dairy cows. The present study evaluated the effect of 17β-estradiol (E2) injections on prolactin (PRL) secretion and the mammary gland response to this hormone. Eight mid-lactation cows were used in a crossover design. During each experimental period, the cows were injected daily with either E2 (2.5 mg) or soy oil (2.5 mL; control) for 7 d. For each period, blood and milk samples were collected from d −4 to 14 (relative to the first injection) to measure PRL, insulin-like growth factor-1, and cortisol concentrations. In addition, blood samples were collected during morning milking on d −4, 2, and 7 to determine the milking-induced PRL release. Mammary gland biopsies were collected on the last day of injections. Milk fat samples were collected from d 1 to 7 and on d 14. The mRNA levels of genes encoding proteins related to mammary activity (α-lactalbumin, β-casein, and acetyl-coenzyme A carboxylase), apoptosis (Bax, Bcl2, and caspase-3), PRL receptors (PRLR; long and short forms), signal transducer and activator of transcription 5 (STAT5A and STAT5B), and suppressors of cytokine signaling (SOCS2 and SOCS3) were evaluated by real-time reverse transcription PCR using RNA extracted from milk fat and mammary biopsies. Milk production was decreased moderately (about 9%) by E2 injections during the treatment period. Estradiol injections increased basal PRL levels in serum and milk but did not affect milking-induced PRL release. Estradiol injections increased the plasma concentration of insulin-like growth factor-1 but did not affect cortisol concentration during the treatment period. In mammary tissue, the expression of Bcl2 was downregulated, whereas that of STAT5A and B and the Bax:Bcl2 mRNA ratio was higher during E2 injections. The total STAT5 protein content in mammary tissue was elevated by E2 injections. We found no significant difference observed for the other genes in mammary tissue or milk fat. The present data do not support the contention that E2 injections inhibit milk production by interfering with PRL signaling, but enhanced basal PRL concentration and STAT5 gene expression in mammary tissue.

雌二醇可抑制奶牛的产奶量。本研究评估了17β-雌二醇（E2）注射对催乳素（PRL）分泌和对这种激素的乳腺反应的影响。在交叉设计中使用了八头泌乳中期的母牛。在每个实验期间，每天向母牛注射E2（2.5 mg）或大豆油（2.5 mL；对照）7天。对于每个时期，从d -4到14（相对于第一次注射）采集血液和牛奶样品，以测量PRL，胰岛素样生长因子-1和皮质醇浓度。另外，在早晨挤奶的第-4、2和7天收集血液样品，以确定挤奶诱导的PRL释放。在注射的最后一天收集乳腺活组织检查物。从第1天到第7天以及第14天收集乳脂样品。Bax，Bcl2和caspase-3），PRL受体（PRLR；长短形式），信号转导和转录激活因子5（STAT5A和STAT5B）以及细胞因子信号转导的抑制因子（SOCS2和SOCS3）通过实时逆转录PCR（使用从乳脂和乳腺活检组织中提取的RNA）进行评估）。在治疗期间，通过E2注射，牛奶产量适度下降（约9％）。雌二醇注射增加血清和牛奶中的基础PRL水平，但不影响挤奶诱导的PRL释放。雌二醇注射增加了胰岛素样生长因子-1的血浆浓度，但在治疗期间未影响皮质醇浓度。在乳腺组织中，Bcl2的表达下调，而STAT5A和B以及Bax：Bcl2的表达下调。在E2注射过程中，mRNA比值更高。注射E2可提高乳腺组织中STAT5总蛋白含量。我们发现乳腺组织或乳脂中的其他基因没有观察到显着差异。本数据不支持E2注射通过干扰PRL信号传导抑制乳汁产生的论点，但在乳腺组织中增强了基础PRL浓度和STAT5基因表达。