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Original Article

Anti-oxidative effects of exogenous ganglioside GD1a and GT1b on embryonic developmental competence in pigs

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  • 발행기관
    한국동물생명공학회(구 한국동물번식학회) 바로가기
  • 간행물
    Journal of Animal Reproduction and Biotechnology 바로가기
  • 통권
    Volume. 35 No. 4 (2020.12)바로가기
  • 페이지
    pp.347-356
  • 저자
    Jin-Woo Kim, Hyo-Jin Park, Seul-Gi Yang, Deog-Bon Koo
  • 언어
    영어(ENG)
  • URL
    https://www.earticle.net/Article/A388201

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원문정보

초록

영어
Gangliosides are glycolipids in which oligosaccharide is combined with sialic acids. Our previous studies have suggested an interplay between ganglioside GD1a/GT1b and meiotic maturation capacity in porcine oocyte maturation. Furthermore, ganglioside GD1a and GT1b are known for its antioxidant activity, but it is still unclear whether possible antioxidant role of GD1a and GT1b is involved in porcine embryos development competence during in vitro culture (IVC). Here, the effects of ganglioside GD1a and GT1b on the embryonic developmental competence during in vitro culture of porcine were investigated. The effects of ganglioside GD1a and GT1b on the expression of ST3GAL2 were confirmed during embryos development (2-cell, 4-cell, 8-cell and blastocyst) using immunofluorescent staining (IF). As a result, the fluorescent expression of ST3GAl2 was higher in embryos at 4-8 cells stage than blastocysts. Blastocyst development rate significantly increased in only 0.1 μM GD1a and GT1b treated groups compared with control group. To investigate the cellular apoptosis, we analyzed TUNEL assay. In case of only 0.1 μM GD1a and GT1b treated groups, the total number of cells in blastocyst compared with control group, but there was no significant difference in the rate of apoptotic cells. We identified the intracellular ROS levels using DCF-DA staining. According to the result, ROS production significantly decreased in blastocysts derived from the 0.1 μM GD1a and GT1b treated groups. These results suggest that ganglioside GD1a and GT1b improve the developmental competence of porcine embryos via reduction of intracellular ROS during preimplantation stage.

목차

ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
Chemicals
In vitro maturation (IVM)
In vitro fertilization and culture (IVF & IVC)
Assessment of apoptosis in blastocysts
Measurement of ROS levels
Statistical analysis
RESULTS
Expression of ST3GAL2 protein in embryos during IVC
Effects of ganglioside GD1a and GT1b on embryonic developmental competence in pigs
Cellular apoptosis in blastocysts derived from ganglioside GD1a and GT1b treated embryos
Effects of ganglioside GD1a and GT1b on intracellular ROS levels of porcine embryos
DISCUSSION
CONCLUSION
CONFLICTS OF INTEREST
ACKNOWLEDGEMENTS
AUTHOR CONTRIBUTIONS
AUTHOR’S POSITION AND ORCID NO.
REFERENCES

키워드

GD1a GT1b In vitro culture (IVC) porcine embryo reactive oxygen species (ROS)

저자

  • Jin-Woo Kim [ Department of Biotechnology, College of Engineering, Daegu University, Institute of Infertility, Daegu University, Gyeongsan 38453, Korea ]
  • Hyo-Jin Park [ Department of Biotechnology, College of Engineering, Daegu University, Institute of Infertility, Daegu University, Gyeongsan 38453, Korea ]
  • Seul-Gi Yang [ Department of Biotechnology, College of Engineering, Daegu University, Institute of Infertility, Daegu University, Gyeongsan 38453, Korea ]
  • Deog-Bon Koo [ Department of Biotechnology, College of Engineering, Daegu University, Institute of Infertility, Daegu University, Gyeongsan 38453, Korea ] Corresponding Author

참고문헌

자료제공 : 네이버학술정보

간행물 정보

발행기관

  • 발행기관명
    한국동물생명공학회(구 한국동물번식학회) [The Korean Society of Animal Reproduction and Biotechnology]
  • 설립연도
    1976
  • 분야
    농수해양>축산학
  • 소개
    동물번식생리학, 동물생명공학, 수의학, 인공수정 및 수정란이식을 이용한 동물개량에 관한 이론과 기술의 발전을 통해 학계, 연구계, 산업계 및 양축가 상호간의 협력을 도모함으로써 동물과학발전 및 사회일반의 이익에 기여 한다는 목적을 위해 노력해 나가겠습니다.

간행물

  • 간행물명
    Journal of Animal Reproduction and Biotechnology
  • 간기
    계간
  • pISSN
    2671-4639
  • eISSN
    2671-4663
  • 수록기간
    2019~2025
  • 십진분류
    KDC 527 DDC 636

이 권호 내 다른 논문 / Journal of Animal Reproduction and Biotechnology Volume. 35 No. 4

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