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Effects of chronic heat stress on granulosa cell apoptosis and follicular atresia in mouse ovary

机译:慢性热应激对小鼠卵巢颗粒细胞凋亡和滤泡闭锁的影响

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摘要

Background:Heat stress is known to alter follicular dynamics and granulosa cell function and may contribute to the diminished reproductive efficiency commonly observed in mammals during the summer.Although several investigators have studied heat-induced ovarian injury,few reports have focused on the effects of chronic heat stress on ovarian function and the molecular mechanisms through which it induces ovarian injury.Methods:In Exp.1,48 female mice were assigned to a control or heat-stressed treatment.After exposure to a constant temperature of 25 ℃ for 7,14,21 or 28 d (n=6) or to 42 ℃ for 3 h per d for 7,14,21 or 28 d (n =6),the mice were euthanized and their ovaries were analyzed for follicular atresia,granulosa cell apoptosis,changes in the abundance of HSPT0 protein and serum concentrations of estradiol.In Exp.2,the expression of HSPT0 and aromatase was quantified in antral follicles cultured in vitro at 37 or 42 ℃ for 24 h.In Exp.3,granulosa cells from ovaries maintained at 37 or 41 ℃ for 2 h were analyzed for their expression of HSP70,Bim,caspase-3 and cleaved caspase-3.Results:In Exp.1,body weight and food intake of heat-stressed mice decreased (P < 0.05) compared with control mice while the concentration of estradiol in serum was lower (P < 0.05) in heat-stressed mice than in control mice.Compared with control mice,the percentage of atretic follicles and the number of antral follicles with severe apoptotic signals were increased (P < 0.05) after 21 d of heat-stressed treatment.HSP70 protein was more abundant (P < 0.05) in heat-stressed mice than control mice.In Exp.2,heat stress increased HSP70 and decreased aromatase proteins (P < 0.05) in antral follicles.In Exp.3,TUNEL-positive granulosa cells from heat-stressed ovaries were observed concomitant with a significant increase in HSP70,Bim and cleaved caspase-3 protein.Conclusion:Heat-stress in mice decrease estradiol in serum and aromatase in antral follicles but increased number of atretic follicles and granulosa cell undergoing apoptosis which may explain the decreased fertility commonly observed in heat-stressed animals.
机译:背景:已知热应激会改变卵泡动力学和颗粒细胞功能,并可能导致夏季通常在哺乳动物中观察到的生殖效率下降。尽管一些研究者已经研究了热诱发的卵巢损伤,但很少有报道关注慢性感染的影响。方法:在实验1,48只雌性小鼠中进行了对照或热应激处理。在25℃的恒温下暴露7,14只,21或28 d(n = 6)或42℃每天3 h持续7,14,21或28 d(n = 6),对小鼠实施安乐死并分析其卵巢的滤泡闭锁,颗粒细胞凋亡在实验2中,对体外培养的37或42℃培养24 h的窦房卵泡中HSPT0和芳香化酶的表达进行了定量。在实验3中,来自大鼠的颗粒细胞卵巢维持在37岁或分析41℃2 h HSP70,Bim,caspase-3和裂解的caspase-3的表达。结果:实验1,热应激小鼠的体重和摄食量较对照组降低(P <0.05)。热应激小鼠血清雌二醇浓度低于对照组(P <0.05)。与对照组相比,有严重凋亡信号的闭锁性卵泡百分比和窦性卵泡数目增加(P <0.05)。热应激21 d后,热应激小鼠的HSP70蛋白含量较对照组高(P <0.05)。实验2中,热应激使肛门HSP70含量升高,芳香酶蛋白含量降低(P <0.05)。在实验3中,观察到热应激卵巢中TUNEL阳性的颗粒细胞伴随着HSP70,Bim和裂解的caspase-3蛋白的显着增加。卵泡,但闭锁卵泡和gra的数量增加核细胞经历凋亡,这可能解释了在热应激动物中通常观察到的生育力下降。

著录项

  • 来源
    《畜牧与生物技术杂志(英文版)》 |2017年第1期|57-66|共10页
  • 作者单位

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

    State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China;

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

    State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China;

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

    Laboratory of Animal Embryonic Biotechnology;

    National Engineering Laboratory for Animal Breeding;

    Key Laboratory of Animal Genetics,Breeding, and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China;

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  • 原文格式 PDF
  • 正文语种 eng
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