【摘要】：目的探究穩(wěn)定型SOD(MS-SOD)灌胃對(duì)小鼠非酒精性脂肪肝及糖代謝的改善作用及其可能機(jī)制。方法實(shí)驗(yàn)一:C57小鼠隨機(jī)分為NC組、HFD組、SOD組。NC組給予基礎(chǔ)飼料,其余給予高脂飼料。第8周開(kāi)始,NC組及HFD組給予無(wú)菌水灌胃,SOD組給予MS-SOD溶液灌胃。灌胃每天1次,直至實(shí)驗(yàn)結(jié)束。實(shí)驗(yàn)結(jié)束前進(jìn)行糖代謝檢測(cè)。實(shí)驗(yàn)結(jié)束后取內(nèi)臟組織保存待測(cè),檢測(cè)內(nèi)容包括脂肪肝、肝臟炎癥因子、腸屏障、盲腸內(nèi)容物宏基因組及腸道菌群。實(shí)驗(yàn)二:C57小鼠隨機(jī)分為高脂組、抗生素高脂組及抗生素高脂SOD組,三組小鼠均予以高脂飼料,后兩組給予抗生素處理。實(shí)驗(yàn)第2周開(kāi)始,抗生素高脂SOD組小鼠予以MS-SOD溶液灌胃,其余組別予以無(wú)菌水灌胃,直至實(shí)驗(yàn)結(jié)束。實(shí)驗(yàn)結(jié)束前進(jìn)行糖代謝檢測(cè)。實(shí)驗(yàn)結(jié)束后取內(nèi)臟組織保存待測(cè),檢測(cè)內(nèi)容包括脂肪肝及肝臟免疫因子。實(shí)驗(yàn)三:ob/ob小鼠隨機(jī)分為對(duì)照組及SOD組,正常飼料喂養(yǎng)滿4周后,對(duì)照組小鼠給予無(wú)菌水灌胃,SOD組小鼠給予MS-SOD溶液灌胃。灌胃每天1次,直至實(shí)驗(yàn)結(jié)束。實(shí)驗(yàn)結(jié)束前進(jìn)行糖代謝檢測(cè)。實(shí)驗(yàn)結(jié)束后取內(nèi)臟組織保存待測(cè),檢測(cè)項(xiàng)目包括脂肪肝、肝臟炎癥因子、糞便清蛋白及腸道菌群。結(jié)果實(shí)驗(yàn)一:1、HFD組小鼠腸道細(xì)菌攜帶錳型SOD降低。2、NC組及SOD組小鼠空腹血糖、GTT試驗(yàn)等糖代謝檢測(cè)優(yōu)于HFD組小鼠。3、NC組及SOD組小鼠脂肪肝評(píng)分及肝細(xì)胞cc14、cc18等炎癥因子mRNA表達(dá)低于HFD組小鼠。4、NC組、HFD組及SOD組在反映腸道菌群β多樣性的PCOA圖中可呈現(xiàn)區(qū)分趨勢(shì)。5、SOD組小鼠腸屏障檢測(cè)測(cè)優(yōu)于HFD組。實(shí)驗(yàn)二:高脂組小鼠在糖代謝、脂肪肝、肝臟炎癥因子檢測(cè)均劣于抗生素高脂組及抗生素高脂SOD組小鼠,但后兩者在各項(xiàng)檢測(cè)中均未見(jiàn)明顯差異。實(shí)驗(yàn)三:1、SOD組小鼠GTT試驗(yàn)等糖代謝檢測(cè)優(yōu)于對(duì)照組;2、SOD組小鼠脂肪肝評(píng)分及肝臟ccl4表達(dá)高于對(duì)照組;3、兩組小鼠腸道菌群存在差異。4、SOD組小鼠糞便清蛋白低于對(duì)照組;結(jié)論實(shí)驗(yàn)一:1、高脂飲食導(dǎo)致小鼠腸道微生攜帶達(dá)錳型SOD降低。2、MS-SOD灌胃可緩解高脂飲食導(dǎo)致小鼠的糖代謝異常、非酒精性脂肪肝炎癥狀,可能機(jī)制為MS-SOD對(duì)腸道菌群及腸道屏障的保護(hù)作用。實(shí)驗(yàn)二:在去除腸道菌群狀態(tài)下,MS-SOD灌胃并未進(jìn)一步促進(jìn)小鼠脂肪肝、糖代謝的改善,提示MS-SOD可能通過(guò)腸道菌群途徑影響相關(guān)代謝。實(shí)驗(yàn)三:MS-SOD能在一定程度上緩解ob/ob小鼠的糖代謝異常及脂肪肝癥狀,保護(hù)腸道屏障及改善腸道菌群。
[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.
【學(xué)位授予單位】：南方醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：R575

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