Serotonin (5-HT) is a monoamine and it could regulate cell growth by its receptors working on signaling pathways. 5-HTP is the precursor of 5-HT that help 5-HT synthesis. B cell leukemia/lymphoma 3 (Bcl-3) involved in cell death and proliferation through mitogen activated protein kinase (MAPK) pathway. However, there is little information about the effects of MAPK/Bcl-3 on apoptosis of goat mammary gland epithelial cell (GMEC). The aim of this study is to explore the interaction among 5-HTP, MAPK and Bcl-3 in GMEC apoptosis. In this study, 5-HTP treatment decreased cell apoptosis and promoted phosphorylation of ERK1/2 in GMEC. We also found that the activation and inhibition of ERK1/2 could affect GMEC apoptosis. The Annexin V-FITC/PI staining and western blotting results suggested that 5-HTP decreased GMEC apoptosis through ERK1/2 signaling pathway. And the results of RT-qPCR and western blotting demonstrated that both 5-HTP and ERK1/2 positively regulated Bcl-3 expression. Sum up all the results, we could draw the conclusion that 5-HTP decreased GMEC apoptosis through MAPK/ERK/Bcl-3 pathway.

血清素（5-HT）是一种单胺，它可以通过其在信号传导途径中起作用的受体来调节细胞的生长。5-HTP是帮助5-HT合成的5-HT的前体。B细胞白血病/淋巴瘤3（Bcl-3）通过有丝分裂原活化蛋白激酶（MAPK）途径参与细胞死亡和增殖。但是，关于MAPK / Bcl-3对山羊乳腺上皮细胞（GMEC）凋亡的影响的信息很少。本研究的目的是探讨5-HTP，MAPK和Bcl-3在GMEC凋亡中的相互作用。在这项研究中，5-HTP处理可降低细胞凋亡并促进GMEC中ERK1 / 2的磷酸化。我们还发现ERK1 / 2的激活和抑制可能影响GMEC凋亡。Annexin V-FITC / PI染色和Western印迹结果表明5-HTP通过ERK1 / 2信号通路减少了GMEC的凋亡。RT-qPCR和western blotting结果表明5-HTP和ERK1 / 2均正调控Bcl-3的表达。综合所有结果，我们可以得出结论：5-HTP通过MAPK / ERK / Bcl-3途径降低了GMEC的凋亡。