运动对肥胖小鼠良性前列腺增生的影响及其机制研究

发布时间：2018-01-18 02:33

本文关键词：运动对肥胖小鼠良性前列腺增生的影响及其机制研究　出处：《上海体育学院》2017年硕士论文　论文类型：学位论文

【摘要】：研究目的本研究以高脂诱导肥胖小鼠前列腺增生为基础,以运动+节食减肥为干预手段,以脂肪细胞因子与性激素为核心,探讨肥胖小鼠诱导前列腺增生的作用机制,为防治肥胖性前列腺增生提供新的思路。研究方法C57BL/6J小鼠80只,造模阶段普通饮食组有16只进行普通饲料喂养,高脂饮食组有64只小鼠经过8周高脂饮食后有38只小鼠达到肥胖标准,即为肥胖组。普通饮食组和高脂饮食组各取8只小鼠作为对照组和肥胖组,解剖取材,分析其糖脂代谢指标以及前列腺增生相关指标。然后进行运动和饮食干预实验。其分组为对照组、节食组、运动+节食组各8只。所有小鼠进行普通饲料喂养,运动方案为小鼠跑台运动,12米/分钟,60分钟,每周6天,共6周。运动结束解剖取材,用酶联免疫法检测糖脂水平和性激素水平;HE染色检测前列腺组织病理变化;悬液芯片检测脂肪细胞因子水平;免疫组化检测雌激素受体蛋白水平。统计方法为独立样本t检验、单因素方差分析以及pearson相关性分析,实验结果以(?)±s表示,r为相关性,显著性水平为P0.05。研究结果1、肥胖组有60%即38只小鼠达到肥胖标准。肥胖组小鼠体重、内脏脂肪重量明显大于对照组(P0.05),血糖升高,血脂水平增加,糖脂代谢水平发生紊乱;2、肥胖组小鼠前列腺重量、前列腺指数、前列腺体积大于对照组,组间具有统计学差异(P0.05)。前列腺腺腔面积和上皮高度均大于对照组,两组具有统计学差异(P0.05)。病理学检查中,对照组小鼠前列腺无增生相关的变化特点。肥胖组小鼠前列腺上皮细胞呈柱状、高柱状,腺腔面积增加,腺上皮高度增加。大量乳头状增生突向腺腔内,腺腔内可见分泌物,腺体周围附着大量脂肪组织。肥胖小鼠发生前列腺增生。3、肥胖组E2/T比值大于对照组,具有统计学差异(P0.05)。Pearson相关性分析显示,各组内的血糖、血脂水平以及内脏脂肪与前列腺体积、前列腺指数都无相关性(P0.05)。4、运动干预:运动+节食组体重、内脏脂肪重量明显减小,而节食组没有明显改善,三组间糖脂水平无差异,运动和低脂的膳食搭配能更好地改善肥胖小鼠体重、内脏脂肪重量以及糖脂代谢水平。5、运动+节食组小鼠前列腺重量、前列腺指数、前列腺体积都要明显的小于节食组(P0.05),与对照组相比无明显的差异。病理学检查中,节食组小鼠前列腺基质层较厚,大量乳头状增生突向腺腔内,腺腔内可见分泌物。运动+节食组病理学检测发现小鼠前列腺增生症状得到良好的改善。说明运动和节食干预更能改善肥胖小鼠前列腺增生症状。6、Pearson相关性分析发现内脂素与前列腺体积呈明显相关性(P0.05),其他各指标无相关性。并且运动+节食组小鼠脂肪细胞因子内脂素水平、抵抗素水平低于节食组,有统计学差异(P0.05),与对照组相比无明显的差异(P0.05)。胰高血糖素水平三组之间无显著性差异(P0.05)。7、小鼠血清雌二醇、睾酮、雌二醇/睾酮比值各指标组间无差异(P0.05)。改善了雌雄激素比例,调整了雌激素受体α和β水平。研究结论肥胖会诱导小鼠前列腺发生增生的病理变化,中等强度的运动和节食干预可以减轻小鼠体重,减少脂肪细胞因子的分泌,调节机体的性激素水平,抑制前列腺增生。
[Abstract]:The study on high fat induced obese mice prostatic hyperplasia based on exercise + diet to lose weight as a means of intervention to Adipocyte Factor and sex hormone as the core, to explore the mechanism of obesity in mice induced by prostatic hyperplasia, to provide new ideas for the prevention and treatment of obesity of prostate hyperplasia. Methods 80 C57BL/6J mice made die stage normal diet group 16 rats was fed with normal diet, high fat diet group and 64 mice with high fat diet for 8 weeks after the 38 mice were obese, as obesity group. Normal diet group and high-fat diet group from each of 8 mice served as control group and obesity group, anatomical specimens analysis of the lipid metabolism index and BPH related indicators. Then exercise and diet intervention experiment. The group as the control group, diet group, exercise + diet group with 8 rats in each group. All mice were fed with normal diet, exercise prescription In the case of treadmill exercise, 12 meters / minute, 60 minutes, 6 days a week, for 6 weeks. The end of the exercise anatomy materials, using enzyme-linked immunosorbent assay, lipid level and sex hormone level; HE staining was used to detect the pathological changes of prostate tissue suspension chip; adipocytokine levels detection; immunohistochemical detection of estrogen receptor protein level. Statistical methods for independent samples t test, ANOVA and Pearson correlation test results to (?) + s said, R correlation, significant level is P0.05. research results of 1, 60% or 38 obese mice reached the standard body weight of obese mice. Obesity, visceral fat weight significantly higher than the control group (P0.05), blood glucose, blood lipid level increased, the level of glucose and lipid metabolism disorders; 2, obese mice prostate weight, prostate index, prostate volume is larger than that of the control group, with statistical difference between groups (P0.05). The prostate gland Cavity area and epithelial height were higher than the control group, with statistical difference between the two groups (P0.05). The pathological examination, the control group did not change the characteristics of mouse prostatic hyperplasia. The obese mice prostate epithelial cells are columnar, columnar, luminal area increased, on the high degree increased. A large number of gland papillary hyperplasia the glandular cavity protruding into the lumen of gland secretions, visible, glands attached to the periphery of the amount of adipose tissue in obese mice. The prostate hyperplasia.3, obesity group E2/T ratio higher than the control group, with statistical difference (P0.05).Pearson correlation analysis showed that each group of blood glucose, blood lipid levels and visceral fat and prostate volume, prostate index had no correlation (P0.05.4), exercise intervention: exercise + diet group body weight, visceral fat weight decreased significantly, while the diet group had no obvious improvement, no differences between the three groups of glucose and lipid level, exercise and low-fat diet collocation To better improve the obese mice body weight, visceral fat weight and lipid metabolism level.5, exercise + diet group mice prostate weight, prostate index, prostate volume was significantly smaller than the diet group (P0.05), compared with the control group had no significant difference. The pathological examination, diet group mice prostatic stromal layers thick, large papillary hyperplasia protruding into the lumen of gland, glandular cavity visible secretions. Pathological examination found that the group of benign prostatic hyperplasia in mice improved exercise + diet. Exercise and diet intervention can improve the symptoms of prostate hyperplasia in obese mice.6, Pearson correlation analysis showed that visfatin and prostate volume were significantly correlated (P0.05), no correlation all the other indexes. And exercise + diet group mice adipocytokine visfatin levels, resistin levels below the dieting group, there were significant differences (P0.05), and control group. No obvious difference ratio (P0.05). Glucagon levels were not significantly different between the three groups (P0.05.7), serum estradiol, testosterone, estradiol / testosterone ratio of each index no difference between groups (P0.05). To improve the proportion of male and female hormones, adjust the estrogen receptor alpha and beta level. Conclusion obesity will happen pathological changes of mice induced by prostate hyperplasia, moderate intensity exercise and diet intervention can reduce weight, reduce the secretion of adipokines, sex hormones regulate the body, inhibit the hyperplasia of prostate.

【学位授予单位】：上海体育学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R697.3;G804.7

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