Insufficient experimental studies have reported the effect of ovalbumin (OVA) as an allergen towards embryonic growth in asthma mouse model. The impact of 10 μg/200 μL OVA on maternal inflammatory and oxidative stress (OS) responses, and preimplantation embryonic development was investigated in this study. We first established OVA-induced asthma mouse model, and following superovulation, mated the females and challenged them with Methacholine (Mch) test. Upon embryo retrieval, only those with the highest implantation potential were cultured in vitro. Significant reduction in the number of embryos at each preimplantation stage was noted in the treated group. Uneven sized blastomeres at 2-, 4- and 8-cell stages were also evident in this group. Embryo fragmentation was significant at only 2-, 4- and 8-cell stages. We also found that OVA tended to raise maternal inflammatory and OS biomarker levels as well as to cause inappropriate levels of pregnancy hormones progesterone (P₄) and estrogen (E₂) although insignificant. The combined results indicate that 10 μg/200 μL OVA had altered both quality and quantity of the embryos in asthma mouse model although its effect on pregnancy hormones, inflammatory and OS responses were non-pathological.

不足的实验研究报告了卵清蛋白 (OVA) 作为过敏原对哮喘小鼠模型胚胎生长的影响。本研究调查了 10 μg/200 μL OVA 对母体炎症和氧化应激 (OS) 反应以及植入前胚胎发育的影响。我们首先建立了OVA诱导的哮喘小鼠模型，并在超数排卵后，将雌性交配并用乙酰甲胆碱（Mch）测试对其进行挑战。在取胚时，只有那些具有最高植入潜力的人才被体外培养。在治疗组中注意到每个植入前阶段的胚胎数量显着减少。在该组中，在 2、4 和 8 细胞阶段的不均匀大小的卵裂球也很明显。胚胎破碎仅在 2、4 和 8 细胞阶段显着。我们还发现 OVA 倾向于提高母体炎症和 OS 生物标志物水平，并导致不适当的妊娠激素黄体酮 (P ₄ ) 和雌激素 (E ₂ )，尽管无关紧要。综合结果表明，10 μg/200 μL OVA 改变了哮喘小鼠模型中胚胎的质量和数量，尽管其对妊娠激素、炎症和 OS 反应的影响是非病理性的。