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首页> 外文期刊>International Journal of Reproductive Medicine >Selenium Attenuates HPV-18 Associated Apoptosis in Embryo-Derived Trophoblastic Cells but Not Inner Cell Mass In Vitro
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Selenium Attenuates HPV-18 Associated Apoptosis in Embryo-Derived Trophoblastic Cells but Not Inner Cell Mass In Vitro

机译：硒在胚胎来源的滋养细胞中减弱HPV-18相关的凋亡，但在体外却没有细胞内质量。

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Objectives. Human papillomaviruses (HPV) are associated with cell cycle arrest. This study focused on antioxidant selenomethionine (SeMet) inhibition of HPV-mediated necrosis. The objectives were to determine HPV-18 effects on embryonic cells and to evaluate SeMet in blocking HPV-18 effects.Methods. Fertilized mouse embryos were cultured for 5 days to implanted trophoblasts and exposed to either control medium (group 1), HPV-18 (group 2), combined HPV-18 and 0.5 µM SeMet (group 3), or combined HPV-18 and 5.0 µM SeMet (group 4). After 48 hrs, trophoblast integrity and, apoptosisecrosis were assessed using morphometric and dual-stain fluorescence assays, respectively.Results. HPV-18 exposed trophoblasts nuclei (253.8 ± 28.5 sq·µ) were 29% smaller than controls (355.6 ± 35.9 sq·µ). Supplementation with 0.5 and 5.0 µM SeMet prevented nuclear shrinkage after HPV-18 exposure. HPV-18 infected trophoblasts remained larger with SeMet supplementation. HPV-18 decreased cell viability by 44% but SeMet supplementation sustained cell viability. Apoptosis was lower when SeMet was present. HPV-18 decreased inner cell mass (ICM) viability by over 60%.Conclusions. HPV-18 decreased nuclear size and trophoblast viability but these effects were attenuated by the antioxidant SeMet. SeMet blocked HPV-18 associated apoptosis process in trophoblasts but not ICM cells suggesting involvement of different oxidative stress pathways.
机译：目标。人乳头瘤病毒（HPV）与细胞周期停滞有关。这项研究的重点是抗氧化剂硒代蛋氨酸（SeMet）抑制HPV介导的坏死。目的是确定HPV-18对胚胎细胞的作用，并评估SeMet在阻断HPV-18作用中的作用。将受精的小鼠胚胎培养5天，植入植入的滋养细胞，并暴露于对照培养基（第1组），HPV-18（第2组），HPV-18和0.5μmMSeMet联合使用（第3组）或HPV-18和5.0联合使用µM SeMet（第4组）。 48小时后，分别使用形态计量学和双重染色荧光检测法评估滋养细胞的完整性和凋亡/坏死。 HPV-18暴露的滋养层细胞核（253.8±28.5 sq·µ）比对照组（355.6±35.9 sq·µ）小29％。补充0.5和5.0μmSeMet可以防止HPV-18暴露后核收缩。补充SeMet后，HPV-18感染的滋养细胞仍较大。 HPV-18使细胞生存力降低了44％，但是补充SeMet可以维持细胞生存力。存在SeMet时，细胞凋亡降低。 HPV-18使内部细胞团（ICM）活力降低了60％以上。 HPV-18减少了核的大小和滋养层的活力，但抗氧化剂SeMet减弱了这些作用。 SeMet阻断了滋养细胞中与HPV-18相关的凋亡过程，但未阻止ICM细胞，提示其参与了不同的氧化应激途径。

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