复合营养素食对Ob/Ob小鼠非酒精性脂肪性肝病的作用及SIRT1/FOXO1通路的影响
发布时间:2021-08-31 21:30
目的观察复合营养素食对Ob/Ob小鼠非酒精性脂肪肝病实验模型的作用及探讨其对于SIRT1/FOXO1通路的影响机制。方法SPF级健康48周龄雄性C57BL/6小鼠、Ob/Ob小鼠各20只,适应性喂养1周后采用随机数字表法平均分为4组:正常对照组、正常素食组、模型组对照组、模型素食组。正常对照组及模型对照组采用小鼠普通维持饲料喂养,正常素食组及模型素食组采用复合营养素食喂养,每周记录摄食量、体重。干预1个月和3个月,采取随机取样法分两批处理,每组各取5只小鼠处死。测量体重、身长,计算体质指数。分离肝脏称肝湿重,计算肝指数。留取血清检测谷草转氨酶(AST),谷丙转氨酶(ALT),胆固醇(CHOL)。留取左叶肝脏部分肝脏组织行H&E、油红O染色及Masson染色,观察肝脏组织脂肪变、气球样变、炎症及纤维化病理变化,以NAFLD的SAF评分定量分析病理程度。留取右叶肝脏部分组织,采用RT-PCR法检测SIRT1mRNA表达水平,采用Western blot法检测SIRT1、AC-FOXO1蛋白水平,采用CO-IP法检测SIRT1与FOXO1之间的相互作用。进行相关...
【文章来源】:南华大学湖南省
【文章页数】:87 页
【学位级别】:硕士
【部分图文】:
各组小鼠摄食
第3章结果21AB模型对照组模型素食组正常对照组正常素食组C图3.2复合营养素食对体重影响。(A)小鼠体重;(B)小鼠外观体型;(C)小鼠体重增长曲线。θθP<0.01vs.干预1月正常对照组,##P<0.01vs.干预3月正常对照组,ΦΦP<0.01vs.干预3月模型对照组3.1.3体质量指数各组小鼠体质量指数比较,数据结果显示:复合营养素食干预1月,与正常对照组相比,模型对照组体质量指数均明显上升(5.49±0.41vs2.83±0.21),差异有统计学意义(t=12.926,P<0.01),正常素食组体质量指数无明显差异(3.01±0.25vs2.83±0.21;t=1.221,P>0.05);与模型对照组相比,模型素食组体质量指数呈下降趋势(5.33±0.28vs5.49±0.41),但差异无统计学意义(t=0.702,P>0.05)。
南华大学硕士学位论文22复合营养素食干预3月,与正常对照组相比,模型对照组体质量指数均明显上升(6.55±0.48vs2.91±0.26),差异有统计学意义(t=14.899,P<0.01),正常素食组体质量指数无明显差异(2.99±0.05vs2.91±0.26;t=0.78,P>0.05);与模型对照组相比,模型素食组体质量指数明显下降(5.37±0.21vs6.55±0.48),差异有统计学意义(t=5.048,P<0.01)。(见表3-2,图3.3)表3-2各组小鼠体质量指数(X±s,kg/m2)组别干预1月干预3月正常对照组(n=5)2.83±0.212.91±0.26正常素食组(n=5)3.01±0.252.99±0.05模型对照组(n=5)5.49±0.416.55±0.48模型素食组(n=5)5.33±0.285.37±0.21图3.3复合营养素食对体质量指数影响。θθP<0.01vs.干预1月正常对照组,##P<0.01vs.干预3月正常对照组,ΦΦP<0.01vs.干预3月模型对照组3.1.4肝湿重各组小鼠肝湿重比较,数据结果显示:复合营养素食干预1月,与正常对照组相比,模型对照组肝湿重明显上升(3.45±0.45vs1.04±0.17),差异有统计学意义(t=11.2,P<0.01),正常素食组肝湿重无明显差异(1.11±0.1vs1.04±0.17;t=0.729,P>0.05);与模型对照组相比,模型素食组肝湿重有所下降(3.14±0.64vs3.45±0.45),但差异无统计学意义(t=0.859,P>0.05)。
【参考文献】:
期刊论文
[1]Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver disease via the Sirt1/AMPK and NF-κB signaling pathways[J]. Chun-Xiao Li,Jian-Guo Gao,Xing-Yong Wan,Yi Chen,Cheng-Fu Xu,Ze-Min Feng,Hang Zeng,Yi-Ming Lin,Han Ma,Ping Xu,Chao-Hui Yu,You-Ming Li. World Journal of Gastroenterology. 2019(34)
[2]Nonalcoholic steatohepatitis severity is defined by a failure in compensatory antioxidant capacity in the setting of mitochondrial dysfunction[J]. Michelle L Boland,Stephanie Oldham,Brandon B Boland,Sarah Will,Jean-Martin Lapointe,Silvia Guionaud,Christopher J Rhodes,James L Trevaskis. World Journal of Gastroenterology. 2018(16)
[3]Metabolic and hepatic effects of liraglutide, obeticholic acid and elafibranor in diet-induced obese mouse models of biopsy-confirmed nonalcoholic steatohepatitis[J]. Kirstine S T?lb?l,Maria NB Kristiansen,Henrik H Hansen,Sanne S Veidal,Kristoffer TG Rigbolt,Matthew P Gillum,Jacob Jelsing,Niels Vrang,Michael Feigh. World Journal of Gastroenterology. 2018(02)
[4]Effectiveness of exercise in hepatic fat mobilization in nonalcoholic fatty liver disease: Systematic review[J]. Pegah Golabi,Cameron T Locklear,Patrick Austin,Sophie Afdhal,Melinda Byrns,Lynn Gerber,Zobair M Younossi. World Journal of Gastroenterology. 2016(27)
[5]Understanding the pathophysiological mechanisms in the pediatric non-alcoholic fatty liver disease: The role of genetics[J]. Pierluigi Marzuillo,Anna Grandone,Laura Perrone,Emanuele Miraglia del Giudice. World Journal of Hepatology. 2015(11)
[6]Pediatric fatty liver disease:Role of ethnicity and genetics[J]. Pierluigi Marzuillo,Emanuele Miraglia del Giudice,Nicola Santoro. World Journal of Gastroenterology. 2014(23)
[7]Association between UCP3 gene polymorphisms and nonalcoholic fatty liver disease in Chinese children[J]. Yan-Ping Xu,Li Liang,Chun-Lin Wang,Jun-Fen Fu,Pei-Ning Liu,Lan-Qiu Lv,Yi-Min Zhu. World Journal of Gastroenterology. 2013(35)
本文编号:3375647
【文章来源】:南华大学湖南省
【文章页数】:87 页
【学位级别】:硕士
【部分图文】:
各组小鼠摄食
第3章结果21AB模型对照组模型素食组正常对照组正常素食组C图3.2复合营养素食对体重影响。(A)小鼠体重;(B)小鼠外观体型;(C)小鼠体重增长曲线。θθP<0.01vs.干预1月正常对照组,##P<0.01vs.干预3月正常对照组,ΦΦP<0.01vs.干预3月模型对照组3.1.3体质量指数各组小鼠体质量指数比较,数据结果显示:复合营养素食干预1月,与正常对照组相比,模型对照组体质量指数均明显上升(5.49±0.41vs2.83±0.21),差异有统计学意义(t=12.926,P<0.01),正常素食组体质量指数无明显差异(3.01±0.25vs2.83±0.21;t=1.221,P>0.05);与模型对照组相比,模型素食组体质量指数呈下降趋势(5.33±0.28vs5.49±0.41),但差异无统计学意义(t=0.702,P>0.05)。
南华大学硕士学位论文22复合营养素食干预3月,与正常对照组相比,模型对照组体质量指数均明显上升(6.55±0.48vs2.91±0.26),差异有统计学意义(t=14.899,P<0.01),正常素食组体质量指数无明显差异(2.99±0.05vs2.91±0.26;t=0.78,P>0.05);与模型对照组相比,模型素食组体质量指数明显下降(5.37±0.21vs6.55±0.48),差异有统计学意义(t=5.048,P<0.01)。(见表3-2,图3.3)表3-2各组小鼠体质量指数(X±s,kg/m2)组别干预1月干预3月正常对照组(n=5)2.83±0.212.91±0.26正常素食组(n=5)3.01±0.252.99±0.05模型对照组(n=5)5.49±0.416.55±0.48模型素食组(n=5)5.33±0.285.37±0.21图3.3复合营养素食对体质量指数影响。θθP<0.01vs.干预1月正常对照组,##P<0.01vs.干预3月正常对照组,ΦΦP<0.01vs.干预3月模型对照组3.1.4肝湿重各组小鼠肝湿重比较,数据结果显示:复合营养素食干预1月,与正常对照组相比,模型对照组肝湿重明显上升(3.45±0.45vs1.04±0.17),差异有统计学意义(t=11.2,P<0.01),正常素食组肝湿重无明显差异(1.11±0.1vs1.04±0.17;t=0.729,P>0.05);与模型对照组相比,模型素食组肝湿重有所下降(3.14±0.64vs3.45±0.45),但差异无统计学意义(t=0.859,P>0.05)。
【参考文献】:
期刊论文
[1]Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver disease via the Sirt1/AMPK and NF-κB signaling pathways[J]. Chun-Xiao Li,Jian-Guo Gao,Xing-Yong Wan,Yi Chen,Cheng-Fu Xu,Ze-Min Feng,Hang Zeng,Yi-Ming Lin,Han Ma,Ping Xu,Chao-Hui Yu,You-Ming Li. World Journal of Gastroenterology. 2019(34)
[2]Nonalcoholic steatohepatitis severity is defined by a failure in compensatory antioxidant capacity in the setting of mitochondrial dysfunction[J]. Michelle L Boland,Stephanie Oldham,Brandon B Boland,Sarah Will,Jean-Martin Lapointe,Silvia Guionaud,Christopher J Rhodes,James L Trevaskis. World Journal of Gastroenterology. 2018(16)
[3]Metabolic and hepatic effects of liraglutide, obeticholic acid and elafibranor in diet-induced obese mouse models of biopsy-confirmed nonalcoholic steatohepatitis[J]. Kirstine S T?lb?l,Maria NB Kristiansen,Henrik H Hansen,Sanne S Veidal,Kristoffer TG Rigbolt,Matthew P Gillum,Jacob Jelsing,Niels Vrang,Michael Feigh. World Journal of Gastroenterology. 2018(02)
[4]Effectiveness of exercise in hepatic fat mobilization in nonalcoholic fatty liver disease: Systematic review[J]. Pegah Golabi,Cameron T Locklear,Patrick Austin,Sophie Afdhal,Melinda Byrns,Lynn Gerber,Zobair M Younossi. World Journal of Gastroenterology. 2016(27)
[5]Understanding the pathophysiological mechanisms in the pediatric non-alcoholic fatty liver disease: The role of genetics[J]. Pierluigi Marzuillo,Anna Grandone,Laura Perrone,Emanuele Miraglia del Giudice. World Journal of Hepatology. 2015(11)
[6]Pediatric fatty liver disease:Role of ethnicity and genetics[J]. Pierluigi Marzuillo,Emanuele Miraglia del Giudice,Nicola Santoro. World Journal of Gastroenterology. 2014(23)
[7]Association between UCP3 gene polymorphisms and nonalcoholic fatty liver disease in Chinese children[J]. Yan-Ping Xu,Li Liang,Chun-Lin Wang,Jun-Fen Fu,Pei-Ning Liu,Lan-Qiu Lv,Yi-Min Zhu. World Journal of Gastroenterology. 2013(35)
本文编号:3375647
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