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K 和 Ca 通道参与了硫化氢抑制猪卵母细胞衰老。

Involvement of K and Ca channels in hydrogen sulfide-suppressed ageing of porcine oocytes.

机构信息

Biomedical Center, Faculty of Medicine in Pilsen, Charles University, alej Svobody 1655/76, Pilsen, Czech Republic.

Department of Histology and Embryology, Faculty of Medicine in Pilsen, Charles University, Pilsen, Czech Republic.

出版信息

Biol Res. 2018 Oct 5;51(1):38. doi: 10.1186/s40659-018-0187-2.

DOI:10.1186/s40659-018-0187-2
PMID:30290763
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6172760/
Abstract

BACKGROUND

Hydrogen sulfide has been shown to improve the quality of oocytes destined for in vitro fertilization. Although hydrogen sulfide is capable of modulating ion channel activity in somatic cells, the role of hydrogen sulfide in gametes and embryos remains unknown. Our observations confirmed the hypothesis that the K and L-type Ca ion channels play roles in porcine oocyte ageing and revealed a plausible contribution of hydrogen sulfide to the modulation of ion channel activity.

RESULTS

We confirmed the benefits of the activation and suppression of the K and L-type Ca ion channels, respectively, for the preservation of oocyte quality.

CONCLUSIONS

Our experiments identified hydrogen sulfide as promoting the desired ion channel activity, with the capacity to protect porcine oocytes against cell death. Further experiments are needed to determine the exact mechanism of hydrogen sulfide in gametes and embryos.

摘要

背景

已有研究表明，硫化氢可提高体外受精卵母细胞的质量。虽然硫化氢能够调节体细胞中的离子通道活性，但硫化氢在配子和胚胎中的作用尚不清楚。我们的观察结果证实了 K 和 L 型钙离子通道在猪卵母细胞衰老过程中起作用的假说，并揭示了硫化氢对离子通道活性调节的可能作用。

结果

我们证实了分别激活和抑制 K 和 L 型钙离子通道对保持卵母细胞质量的益处。

结论

我们的实验确定了硫化氢能促进所需的离子通道活性，从而保护猪卵母细胞免于细胞死亡。需要进一步的实验来确定硫化氢在配子和胚胎中的确切作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/09a37447a1a5/40659_2018_187_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/c731ee7ce71f/40659_2018_187_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/09e5f23bcc52/40659_2018_187_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/d0f1e8cc3ca2/40659_2018_187_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/d527e72bfd40/40659_2018_187_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/09a37447a1a5/40659_2018_187_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/c731ee7ce71f/40659_2018_187_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/09e5f23bcc52/40659_2018_187_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/d0f1e8cc3ca2/40659_2018_187_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/d527e72bfd40/40659_2018_187_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9007/6172760/09a37447a1a5/40659_2018_187_Fig5_HTML.jpg

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Oxid Med Cell Longev. 2016;2016:1730750. doi: 10.1155/2016/1730750. Epub 2016 Aug 8.
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