摘要
目的探究高脂饮食诱导的肥胖引起C57BL/6小鼠精子线粒体损伤及活动力低下的作用机制。方法构建肥胖实验动物模型。采用计算机辅助精液分析仪(computer-assisted semen analysis, CASA)分析其生育力相关参数,包括精子活动力、前向运动精子百分数以及精子浓度;运用苏木精-伊红染色法(hematoxylin-eosin staining, HE)分析正常与肥胖小鼠的睾丸形态学结构,荧光探针JC-1和罗丹明123对小鼠精子线粒体进行染色,采用流式细胞仪分析两组精子染色后的平均荧光强度,最后使用Real-time PCR对两组小鼠精子线粒体DNA(mitochondrial DNA, mtDNA)的拷贝数进行分析。结果与正常野生型小鼠相比,肥胖小鼠的精子活动力、前向运动精子百分数明显减弱且睾丸形态存在异常,而精子浓度没有明显变化。进一步研究发现,与正常小鼠相比,肥胖小鼠的精子线粒体膜电位显著降低,但两者mtDNA拷贝数没有明显差异。结论肥胖能够引起精子线粒体功能损伤从而导致精子活动力及前向运动精子百分数低下,最终损伤雄性的生殖功能。
Objective To explore the mechanism of mitochondrial injury and lower decreased sperm motility of sperm caused by high fat diet (HFD)-induced obesity induced by high fat diet (HFD) in C57BL/6 mice. Methods Animal models with Oobesity animal model were establishedas generated by HFD feeding. Computer-assisted semen analyzer was used to analyze the sperm parameters of fertility, including the ratio of sperm motility, progressive motility and sperm concentration. The HE staining was employed to detect testicular morphology of obese mice, the HE staining was performed and fluorescent probes JC? 1 and Rhodamine 123 were used to stain sperm mitochondria and the average fluorescence intensity of staining was measuredanalyze via by flow cytometry. Real-time PCR was used to evaluate the copy number of sperm mitochondrial DNA. Results Compared with that of the control groupmice, the sperm motility and progressive motility of sperm in obese mice group were significantly decreased, and the testicular morphology was severely impaired. buBut no significant change was found in sperm concentrationthere was no significant difference in sperm concentration. The testicular morphology of obese mice was severe impaired. AdditionallyCompared with control mice,, the sperm mitochondrial membrane potential of sperm in obese mice group was also significantly decreased, but there was nno significant changedifference in the number of mtDNA copies between these twogroups. Conclusion Obesity can impair sperm mitochondrial function, in turn resulting in lower sperm motility and progressive motility, ultimately thereby injurempairing male reproductive function.
作者
彭媛红
敬佳
胡燕琴
刘悦
丁之德
Peng Yuanhong;Jing Jia;Hu Yanqin;Liu Yue;Ding Zhide(Department of Histology, Embryology, Genetics and Developmental Biology Shanghai Key Laboratory of Reproductive Medicine)
出处
《中国男科学杂志》
CAS
CSCD
2019年第3期3-9,共7页
Chinese Journal of Andrology
