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硫氧还蛋白通过促进大鼠孕酮生成在体外刺激黄体化。

Sulfiredoxin stimulates luteinization in vitro by promoting progesterone production in rats.

作者信息

Chun Sang-Young, Park Eun-Hye, Jang Mari, Park Jae-Il, Jang You-Jee

机构信息

School of Biological Sciences & Technology, Faculty of Life Science, Chonnam National University, Gwangju, Republic of Korea.

Department of Biomedical Laboratory Science, Honam University, Gwangju, Republic of Korea.

出版信息

Reproduction. 2025 Sep 19;170(4). doi: 10.1530/REP-25-0066. Print 2025 Oct 1.

DOI:10.1530/REP-25-0066
PMID:40891754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12449702/
Abstract

IN BRIEF

Sulfiredoxin (Srxn1) is essential for corpus luteum formation during ovulation. Inhibition of Srxn1 with J14 suppressed LH-stimulated progesterone production, key gene expressions (Cyp11a1, Star), and markers of luteinization. This highlights Srxn1's role in promoting LH-induced luteinization through the ERK, C/EBPβ, and Cyp11a1 pathways.

ABSTRACT

Sulfiredoxin (Srxn1), an antioxidant enzyme, is expressed during ovulation. This study aimed to investigate the physiological function of Srxn1 in corpus luteum formation during the ovulatory process in rats. Treatment of cultured preovulatory follicles with the Srxn1 inhibitor, J14, suppressed LH-stimulated progesterone production, but not estradiol production, in a dose-dependent manner. Likewise, LH-stimulated gene expression of Cyp11a1 and Star, but not Cyp19a1, was suppressed by J14. Regulation of Cyp11a1 and STAR expression by Srxn1 was confirmed using si-Srxn1 in KGN cells, a human granulosa cell line. Furthermore, treatment of preovulatory granulosa cells with J14 dose-dependently suppressed LH-stimulated mRNA and protein levels of C/EBPβ and ERK1/2. Finally, hypertrophy, lipid droplets, progesterone production, and p27Kip1 expression stimulated by LH were significantly lowered by J14 in in vitro luteinization of granulosa cells. Taken together, the present data indicate that Srxn1 plays a significant role in the formation of the corpus luteum during ovulation by stimulating the pathways of ERK, C/EBPβ, and Cyp11a1.

摘要

简而言之

硫氧还蛋白(Srxn1)在排卵期间的黄体形成过程中至关重要。用J14抑制Srxn1可抑制促黄体生成素(LH)刺激的孕酮生成、关键基因表达(Cyp11a1、Star)以及黄体化标志物。这突出了Srxn1在通过细胞外信号调节激酶(ERK)、C/EBPβ和Cyp11a1途径促进LH诱导的黄体化中的作用。

摘要

硫氧还蛋白(Srxn1)是一种抗氧化酶,在排卵期间表达。本研究旨在探讨Srxn1在大鼠排卵过程中黄体形成的生理功能。用Srxn1抑制剂J14处理培养的排卵前卵泡,以剂量依赖的方式抑制了LH刺激的孕酮生成,但不影响雌二醇生成。同样,J14抑制了LH刺激的Cyp11a1和Star基因表达,但不影响Cyp19a1的表达。在人颗粒细胞系KGN细胞中使用小干扰RNA(si - Srxn1)证实了Srxn1对Cyp11a1和STAR表达的调节作用。此外,用J14处理排卵前颗粒细胞可剂量依赖地抑制LH刺激的C/EBPβ和ERK1/2的mRNA和蛋白水平。最后,在颗粒细胞的体外黄体化过程中,J14显著降低了LH刺激的肥大、脂滴、孕酮生成和p27Kip1表达。综上所述,目前的数据表明Srxn1通过刺激ERK、C/EBPβ和Cyp11a1途径在排卵期间的黄体形成中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/9aa1eaefe8e2/REP-25-0066fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/6ad0ccfe8166/REP-25-0066fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/ea9f02c2b554/REP-25-0066fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/82be11cb9ca0/REP-25-0066fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/e6cca112e77f/REP-25-0066fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/8a4d43e8e6c1/REP-25-0066fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/f14837d40554/REP-25-0066fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/9aa1eaefe8e2/REP-25-0066fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/6ad0ccfe8166/REP-25-0066fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/ea9f02c2b554/REP-25-0066fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/82be11cb9ca0/REP-25-0066fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/e6cca112e77f/REP-25-0066fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/8a4d43e8e6c1/REP-25-0066fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/f14837d40554/REP-25-0066fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1eda/12449702/9aa1eaefe8e2/REP-25-0066fig7.jpg

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Oxidative Stress: The Role of Estrogen and Progesterone.氧化应激:雌激素与孕激素的作用
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Sulfiredoxin-1 enhances cardiac progenitor cell survival against oxidative stress via the upregulation of the ERK/NRF2 signal pathway.硫氧还蛋白-1 通过上调 ERK/NRF2 信号通路增强心肌祖细胞对抗氧化应激的存活能力。
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Sulfiredoxin inhibitor induces preferential death of cancer cells through reactive oxygen species-mediated mitochondrial damage.硫氧还蛋白抑制剂通过活性氧介导的线粒体损伤诱导癌细胞选择性死亡。
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