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黄体生成素作为体外牛黄体细胞凋亡抑制因子的作用。

The effects of luteinizing hormone as a suppression factor for apoptosis in bovine luteal cells in vitro.

机构信息

Cellular and Molecular Mechanisms in Biological System (CEMBIOS) Research Group, Department of Biology, Faculty of Mathematics and Natural Sciences of Universitas Indonesia, Depok, Indonesia.

Department of Diabetes, Endocrinology, and Nutrition, Graduates School of Medicine, Kyoto University, Kyoto, Japan.

出版信息

Reprod Domest Anim. 2021 May;56(5):744-753. doi: 10.1111/rda.13913. Epub 2021 Feb 22.

DOI:10.1111/rda.13913
PMID:33560544
Abstract

The fate of the corpus luteum, a transient endocrine gland formed and degraded during an oestrous cycle, is decided by various physiological factors, such as luteinizing hormone (LH). As a stimulator of progesterone, LH is known to maintain corpus luteum functional and structural integrity by inhibiting apoptosis, a programmed cell death. Therefore, we aim to investigate its action during the mid-luteal phase hypothesized that LH suppresses the death mechanism of bovine luteal steroidogenic cells (LSC) by analysing the expression of proteins involved. Cultured bovine LSC obtained from corpus luteum were treated for 24 hr with recombinant TNF and IFNG in the presence or absence of LH. The result showed that LH proved to have a protective effect by increased cell viability (p < .05) and prevented DNA fragmentation (p < .05), as demonstrated by the WST-1 colorimetric assay and TUNEL assay. Expression analysis of mRNA and protein levels showed that LH altered the expression of BCL2 (p < .05), CASP3 (p < .05), FAS (p < .05), and BAX (p < .05) to support cell survival. In conclusion, our study suggests that LH prolongs the corpus luteum life span through the anti-apoptotic mechanism by increasing cell viability and suppressing apoptosis-related genes and protein expression.

摘要

黄体的命运是由各种生理因素决定的,例如黄体生成素 (LH)。黄体是一种在发情周期中形成和降解的短暂内分泌腺。作为孕激素的刺激物,LH 通过抑制细胞凋亡来维持黄体的功能和结构完整性,细胞凋亡是一种程序性细胞死亡。因此,我们旨在通过分析涉及的蛋白质的表达来研究其在黄体中期的作用,假设 LH 通过抑制黄体类固醇生成细胞 (LSC) 的死亡机制来抑制黄体的死亡机制。培养来自黄体的牛 LSC 在存在或不存在 LH 的情况下用重组 TNF 和 IFNG 处理 24 小时。结果表明,LH 通过增加细胞活力(p<.05)和防止 DNA 片段化(p<.05),通过 WST-1 比色法和 TUNEL 测定证明具有保护作用。mRNA 和蛋白质水平的表达分析表明,LH 改变了 BCL2(p<.05)、CASP3(p<.05)、FAS(p<.05)和 BAX(p<.05)的表达,以支持细胞存活。总之,我们的研究表明,LH 通过增加细胞活力和抑制与凋亡相关的基因和蛋白质表达来延长黄体的寿命,从而发挥抗凋亡作用。

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