稳定型超氧化物歧化酶对小鼠非酒精性脂肪肝及肠道菌群的影响
发布时间：2018-08-11 18:09
【摘要】：目的探究稳定型SOD(MS-SOD)灌胃对小鼠非酒精性脂肪肝及糖代谢的改善作用及其可能机制。方法实验一:C57小鼠随机分为NC组、HFD组、SOD组。NC组给予基础饲料,其余给予高脂饲料。第8周开始,NC组及HFD组给予无菌水灌胃,SOD组给予MS-SOD溶液灌胃。灌胃每天1次,直至实验结束。实验结束前进行糖代谢检测。实验结束后取内脏组织保存待测,检测内容包括脂肪肝、肝脏炎症因子、肠屏障、盲肠内容物宏基因组及肠道菌群。实验二:C57小鼠随机分为高脂组、抗生素高脂组及抗生素高脂SOD组,三组小鼠均予以高脂饲料,后两组给予抗生素处理。实验第2周开始,抗生素高脂SOD组小鼠予以MS-SOD溶液灌胃,其余组别予以无菌水灌胃,直至实验结束。实验结束前进行糖代谢检测。实验结束后取内脏组织保存待测,检测内容包括脂肪肝及肝脏免疫因子。实验三:ob/ob小鼠随机分为对照组及SOD组,正常饲料喂养满4周后,对照组小鼠给予无菌水灌胃,SOD组小鼠给予MS-SOD溶液灌胃。灌胃每天1次,直至实验结束。实验结束前进行糖代谢检测。实验结束后取内脏组织保存待测,检测项目包括脂肪肝、肝脏炎症因子、粪便清蛋白及肠道菌群。结果实验一:1、HFD组小鼠肠道细菌携带锰型SOD降低。2、NC组及SOD组小鼠空腹血糖、GTT试验等糖代谢检测优于HFD组小鼠。3、NC组及SOD组小鼠脂肪肝评分及肝细胞cc14、cc18等炎症因子mRNA表达低于HFD组小鼠。4、NC组、HFD组及SOD组在反映肠道菌群β多样性的PCOA图中可呈现区分趋势。5、SOD组小鼠肠屏障检测测优于HFD组。实验二:高脂组小鼠在糖代谢、脂肪肝、肝脏炎症因子检测均劣于抗生素高脂组及抗生素高脂SOD组小鼠,但后两者在各项检测中均未见明显差异。实验三:1、SOD组小鼠GTT试验等糖代谢检测优于对照组;2、SOD组小鼠脂肪肝评分及肝脏ccl4表达高于对照组;3、两组小鼠肠道菌群存在差异。4、SOD组小鼠粪便清蛋白低于对照组;结论实验一:1、高脂饮食导致小鼠肠道微生携带达锰型SOD降低。2、MS-SOD灌胃可缓解高脂饮食导致小鼠的糖代谢异常、非酒精性脂肪肝炎症状,可能机制为MS-SOD对肠道菌群及肠道屏障的保护作用。实验二:在去除肠道菌群状态下,MS-SOD灌胃并未进一步促进小鼠脂肪肝、糖代谢的改善,提示MS-SOD可能通过肠道菌群途径影响相关代谢。实验三:MS-SOD能在一定程度上缓解ob/ob小鼠的糖代谢异常及脂肪肝症状,保护肠道屏障及改善肠道菌群。
[Abstract]:Objective to investigate the effects of stable SOD (MS-SOD) on non-alcoholic fatty liver and glucose metabolism in mice and its possible mechanism. Methods experiment 1: C57 mice were randomly divided into NC group, HFD group, SOD group. NC group were given basic diet, others were given high fat diet. From the 8th week, the NC group and the HFD group were given MS-SOD solution by gastric perfusion with aseptic water. Once a day until the end of the experiment. Glucose metabolism was detected before the end of the experiment. At the end of the experiment, the visceral tissue was preserved to be tested, including fatty liver, liver inflammatory factors, intestinal barrier, macrogenome of caecum contents and intestinal flora. Experiment 2: C57 mice were randomly divided into high fat group, antibiotic high fat group and antibiotic high fat SOD group. All the three groups were given high fat diet, the latter two groups were treated with antibiotics. From the second week of the experiment, the mice in the high fat SOD group were fed with MS-SOD solution, and the other groups were fed with aseptic water until the end of the experiment. Glucose metabolism was detected before the end of the experiment. At the end of the experiment, the visceral tissue was preserved to be tested, including fatty liver and liver immune factors. Experiment 3: ob-ob mice were randomly divided into two groups: control group and SOD group. After 4 weeks of normal feed feeding, the control group mice were given MS-SOD solution by gastric perfusion with aseptic water. Once a day until the end of the experiment. Glucose metabolism was detected before the end of the experiment. At the end of the experiment, the visceral tissue was preserved to be tested, including fatty liver, liver inflammatory factors, fecal albumin and intestinal flora. Results in experiment 1, the glucose metabolism of intestinal bacteria carrying manganese type SOD decreased in group NC and mice in SOD group was superior to that in group HFD and group SOD in fatty liver score and mRNA table of inflammation factor such as cc14C18 in hepatocytes. The results showed that the glucose metabolism of mice in the control group was better than that in the group of HFD group and the group of SOD group, and that in the control group was better than that in the group of HFD group and the group of SOD mice. Compared with the control group, the HFD group and SOD group showed a distinguishing trend in the PCOA map reflecting the 尾 diversity of intestinal flora. The detection of intestinal barrier was superior to that of the HFD group in the detection of intestinal barrier in the mice with lower than that in the HFD group (.4nc) and the SOD group (P < 0.05). Experiment 2: the detection of glucose metabolism, fatty liver and liver inflammatory factors in hyperlipidemia group were inferior to those in antibiotic hyperlipidemia group and antibiotic hyperlipidemia SOD group, but there was no significant difference between the latter two groups. Experiment 3: 1 sod group was superior to control group in fatty liver score and liver ccl4 expression compared with control group (P < 0.05). There was significant difference in intestinal microflora between the two groups. The fecal albumin in the control group was lower than that in the control group. Conclusion in experiment 1: 1, high fat diet could alleviate the abnormal glucose metabolism and the symptom of non-alcoholic fatty liver disease induced by high fat diet in mice. The possible mechanism is the protective effect of MS-SOD on intestinal flora and intestinal barrier. Experiment 2: under the condition of removing intestinal flora, MS-SOD administration did not further promote the improvement of fatty liver and glucose metabolism in mice, suggesting that MS-SOD may affect the related metabolism through intestinal microflora. Experiment 3: MS-SOD could alleviate abnormal glucose metabolism and fatty liver symptoms of ob/ob mice to some extent, protect intestinal barrier and improve intestinal flora.
【学位授予单位】：南方医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R575
本文编号：2177815
[Abstract]:Objective to investigate the effects of stable SOD (MS-SOD) on non-alcoholic fatty liver and glucose metabolism in mice and its possible mechanism. Methods experiment 1: C57 mice were randomly divided into NC group, HFD group, SOD group. NC group were given basic diet, others were given high fat diet. From the 8th week, the NC group and the HFD group were given MS-SOD solution by gastric perfusion with aseptic water. Once a day until the end of the experiment. Glucose metabolism was detected before the end of the experiment. At the end of the experiment, the visceral tissue was preserved to be tested, including fatty liver, liver inflammatory factors, intestinal barrier, macrogenome of caecum contents and intestinal flora. Experiment 2: C57 mice were randomly divided into high fat group, antibiotic high fat group and antibiotic high fat SOD group. All the three groups were given high fat diet, the latter two groups were treated with antibiotics. From the second week of the experiment, the mice in the high fat SOD group were fed with MS-SOD solution, and the other groups were fed with aseptic water until the end of the experiment. Glucose metabolism was detected before the end of the experiment. At the end of the experiment, the visceral tissue was preserved to be tested, including fatty liver and liver immune factors. Experiment 3: ob-ob mice were randomly divided into two groups: control group and SOD group. After 4 weeks of normal feed feeding, the control group mice were given MS-SOD solution by gastric perfusion with aseptic water. Once a day until the end of the experiment. Glucose metabolism was detected before the end of the experiment. At the end of the experiment, the visceral tissue was preserved to be tested, including fatty liver, liver inflammatory factors, fecal albumin and intestinal flora. Results in experiment 1, the glucose metabolism of intestinal bacteria carrying manganese type SOD decreased in group NC and mice in SOD group was superior to that in group HFD and group SOD in fatty liver score and mRNA table of inflammation factor such as cc14C18 in hepatocytes. The results showed that the glucose metabolism of mice in the control group was better than that in the group of HFD group and the group of SOD group, and that in the control group was better than that in the group of HFD group and the group of SOD mice. Compared with the control group, the HFD group and SOD group showed a distinguishing trend in the PCOA map reflecting the 尾 diversity of intestinal flora. The detection of intestinal barrier was superior to that of the HFD group in the detection of intestinal barrier in the mice with lower than that in the HFD group (.4nc) and the SOD group (P < 0.05). Experiment 2: the detection of glucose metabolism, fatty liver and liver inflammatory factors in hyperlipidemia group were inferior to those in antibiotic hyperlipidemia group and antibiotic hyperlipidemia SOD group, but there was no significant difference between the latter two groups. Experiment 3: 1 sod group was superior to control group in fatty liver score and liver ccl4 expression compared with control group (P < 0.05). There was significant difference in intestinal microflora between the two groups. The fecal albumin in the control group was lower than that in the control group. Conclusion in experiment 1: 1, high fat diet could alleviate the abnormal glucose metabolism and the symptom of non-alcoholic fatty liver disease induced by high fat diet in mice. The possible mechanism is the protective effect of MS-SOD on intestinal flora and intestinal barrier. Experiment 2: under the condition of removing intestinal flora, MS-SOD administration did not further promote the improvement of fatty liver and glucose metabolism in mice, suggesting that MS-SOD may affect the related metabolism through intestinal microflora. Experiment 3: MS-SOD could alleviate abnormal glucose metabolism and fatty liver symptoms of ob/ob mice to some extent, protect intestinal barrier and improve intestinal flora.
【学位授予单位】：南方医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R575
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