Procyanidin B2 Improves Oocyte Maturation and Subsequent Development in Type 1 Diabetic Mice by Promoting Mitochondrial Function

被引:24
|
作者
Luo, Yuxi [1 ]
Zhuan, Qingrui [1 ]
Li, Jun [2 ]
Du, Xingzhu [1 ]
Huang, Zhengyuan [3 ]
Hou, Yunpeng [4 ]
Fu, Xiangwei [1 ]
机构
[1] China Agr Univ, Coll Anim Sci & Technol, Natl Engn Lab Anim Breeding, Beijing Key Lab Anim Genet Improvement, Beijing 100193, Peoples R China
[2] Hebei Med Univ, Hosp 1, Dept Reprod Med, Shijiazhuang 050031, Hebei, Peoples R China
[3] Imperial Coll London, Chelsea & Westminster Hosp, Dept Metab Digest & Reprod, London SW10 9NH, England
[4] China Agr Univ, Coll Biol Sci, State Key Lab Agro Biotechnol, Yuanmingyuan West Rd 2, Beijing 100193, Peoples R China
关键词
Oocyte; Embryo; Procyanidin B2; Mitochondrial; Crotonylation; Mice; ATP CONTENT; HISTONE CROTONYLATION; OXIDATIVE STRESS; GENE-EXPRESSION; IN-VITRO; IDENTIFICATION; DYSFUNCTION; TEMPERATURE; METABOLISM; FERTILITY;
D O I
10.1007/s43032-020-00241-3
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Type 1 diabetes (T1D) results in decreased oocyte quality and compromised early embryonic development. Procyanidin B2 (PB2) is a natural compound extracted from grape seeds and has strong antioxidant activity in vivo. This study evaluated the effect of PB2 on oocyte maturation in diabetic mice. Diabetic mice were induced by streptozotocin (STZ) injection. PB2 was supplemented in the in vitro maturation medium, and the ratio of germinal vesicle breakdown (GVBD) and polar body extrusion (PBE), reactive oxygen species (ROS) levels, mitochondrial function, developmental ability, as well as crotonylation at H4K5 were determined in oocytes. PB2 can promote the extrusion of PBE (88.34% vs. 75.02%,P < 0.05); reduce the generation of ROS (1.12 vs. 1.96,P < 0.05); and improve the level of mitochondrial membrane potential (0.87 vs. 0.79 Delta phi m,P < 0.05), ATP level (1.31 vs. 0.71 pmol,P < 0.05), and mitochondria temperature (618.25 vs. 697.39 pixels,P < 0.05). The addition of PB2 also improved the level of oocyte crotonylation at H4K5 (crH4K5) (47.26 vs. 59.68 pixels,P < 0.05) and increased the blastocyst rate (61.51% vs. 36.07%,P < 0.05) after parthenogenetic activation. Our results are the first to reveal a role for PB2 in promoting the viability of oocytes by regulating the mitochondrial function. Moreover, we uncover that PB2 can improve the level of crH4K5, which provides a new strategy to combat the decline in oocyte quality of diabetic.
引用
收藏
页码:2211 / 2222
页数:12
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