【摘要】 目的:探讨肥胖对雄性小鼠生殖系统的损伤及表观遗传机制。方法:选取2019年10月—2020年6月SPF级雄鼠20只(5周、体重19～20g),随机分为肥胖组和对照组。构建小鼠肥胖模型,取精子进行形态、密度、活力参数及动力参数分析,提取精子残余组蛋白检测H3K56乙酰化程度。结果:肥胖组小鼠精子正常率显著低于对照组(61.32±2.46 vs 83.37±2.87,P<0.05);精子密度及活力参数均显著降低(P<0.05);动力参数除精子平均移动角度,鞭打频率与摆动性之外均低于对照组,有显著差异(P <0.05);残余组蛋白H3K56乙酰化程度显著低于对照组(0.46±0.18 vs 1.03±0.51,P<0.01)。结论:肥胖降低雄性小鼠精子活力、精子密度,增加精子畸形率,干扰精子残余组蛋白乙酰化过程,从而对雄性生殖系统产生影响。更多还原

【Abstract】 Objective To explore the damage of obesity to the reproductive system of male mice and its epigenetic mechanism.Methods From October 2019 to June 2020,20 SPF male rats(5 weeks,19～20 g body weight) were randomly divided into obese group and control group.Mouse obesity model was established.Sperm morphology,density,activity parameters and dynamic parameters were analyzed.Sperm histone residues were extracted to detect the acetylation degree of H3 K56.Results Compared with the control group,there were significant differences in density,morphology rate,motility rate,curve speed,linear speed,average path speed,lateral swing amplitude,linear percentage and forward percentage in obese mice(P <0.05).However,there was no difference in movement angle,flogging frequency and swing percentage(P> 0.05).The acetylation degree of H3 K56 in obese mice was significantly lower(P <0.01).Conclusion Obesity can reduce sperm motility and density in male mice,increase deformity rate,and interfere with the acetylation process of sperm histone.更多还原