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MicroRNA-29b在酒精性肝病中的作用及机制研究

发布时间:2024-05-18 06:20
  背景酒精性肝病(Alcoholic liver disease,ALD)是全球常见的慢性肝病,由于发病率和死亡率逐年升高,已经获得了社会上的广泛关注。饮酒者长期过量摄入酒精后会引起肝脏肝细胞损伤、炎症、氧化应激等,通常还会诱发microRNA(miRNA)表达异常。我们之前的研究表明miR-29b存在于多种肝实质和非实质性细胞中,且与肝纤维化的发展密切相关。过表达miR-29b能够显著抑制胶原沉积,缓解肝纤维化。但是miR-29b对酒精性肝病早期阶段的影响尚不明确,本课题拟采用miR-29b敲除小鼠研究其在酒精性肝病中的作用,并探讨其作用机制。目的研究miR-29b在酒精性肝病中的作用及其机制。方法1.本研究采用野生型(Wide type,WT)小鼠和miR-29b敲除(miR-29b-/-)小鼠构建慢加急性酒精性肝损伤模型(Gao-Binge模型)。2.应用生化分析仪检测对照组与实验组小鼠血清谷草转氨酶(AST)和谷丙转氨酶(ALT)水平,用以衡量酒精性肝损伤的程度。3.取对照组和实验组小鼠的肝组织固定于4%甲醛溶液中,石蜡包埋后切片进行苏木精-伊红(Hemat...

【文章页数】:74 页

【学位级别】:硕士

【部分图文】:

图3.1:Gao-Binge模型中小鼠肝脏miR-29b表达降低Figure3.1.Ethanolfeedinginduceshepaticdown-regulationofmiRNA-29binWTmice.ExpressionofmiR-29bfrom10-dayethanolfeeding(A)liversandonebinge(B)liversofmiceincontrasttocontrol,respectively.n>5pergroup.(C)miR-29blevelsinliversofGao-Bingemouse

图3.1:Gao-Binge模型中小鼠肝脏miR-29b表达降低Figure3.1.Ethanolfeedinginduceshepaticdown-regulationofmiRNA-29binWTmice.ExpressionofmiR-29bfrom10-dayethanolfeeding(A)liversandonebinge(B)liversofmiceincontrasttocontrol,respectively.n>5pergroup.(C)miR-29blevelsinliversofGao-Bingemouse

图3.1:Gao-Binge模型中小鼠肝脏miR-29b表达降低Figure3.1.Ethanolfeedinginduceshepaticdown-regulationofmiRNA-29binWTmice.ExpressionofmiR-29....


图3.3:miR-29b敲除可明显加重酒精诱导的中性粒细胞浸润Figure3.3.Alcohol-inducedhepaticneutrophilinfiltrationandinflammationisexacerbatedinmiRNA-29b-/-mice.(A-B)ThenumberofMPOwascountedpervisualfieldoflivertissuesin

图3.3:miR-29b敲除可明显加重酒精诱导的中性粒细胞浸润Figure3.3.Alcohol-inducedhepaticneutrophilinfiltrationandinflammationisexacerbatedinmiRNA-29b-/-mice.(A-B)ThenumberofMPOwascountedpervisualfieldoflivertissuesin

图3.3:miR-29b敲除可明显加重酒精诱导的中性粒细胞浸润Figure3.3.Alcohol-inducedhepaticneutrophilinfiltrationandinflammationisexacerbatedinmiRNA-29b-/-m....


图3.4:miR-29b敲除可明显加重酒精诱导的肝脏巨噬细胞激活和炎症反应Figure3.4.Alcohol-inducedhepaticmacrophageactivationandinflammationisaggravatedinmiRNA-29b-/-mice.(A)ImmunohistochemistryofF4/80indicatedmacrophageactivation.Scalebarsare20μm.(B)Hepaticgeneexpressionofpro-inflammatorymediators.n>5pergroup.Theresultswereexpressedasthemean±SD,*p<0.05,**p<0.01.

图3.4:miR-29b敲除可明显加重酒精诱导的肝脏巨噬细胞激活和炎症反应Figure3.4.Alcohol-inducedhepaticmacrophageactivationandinflammationisaggravatedinmiRNA-29b-/-mice.(A)ImmunohistochemistryofF4/80indicatedmacrophageactivation.Scalebarsare20μm.(B)Hepaticgeneexpressionofpro-inflammatorymediators.n>5pergroup.Theresultswereexpressedasthemean±SD,*p<0.05,**p<0.01.

313.4:miR-29b敲除可明显加重酒精诱导的肝脏巨噬细胞激活和炎症反应igure3.4.Alcohol-inducedhepaticmacrophageactivationandinflammationisaggravateiRNA-29b-/-mic....


图3.5:miR-29b敲除可明显加重酒精诱导的氧化应激Figure3.5.DepletionofmiR-29bexacerbatesoxidativestressafterchronic-plus-bingeethanolfeeding.(A)Immunohistochemistryof4-HNEintheliversofpair-fedorethanoltreatedmice.n>5

图3.5:miR-29b敲除可明显加重酒精诱导的氧化应激Figure3.5.DepletionofmiR-29bexacerbatesoxidativestressafterchronic-plus-bingeethanolfeeding.(A)Immunohistochemistryof4-HNEintheliversofpair-fedorethanoltreatedmice.n>5

图3.5:miR-29b敲除可明显加重酒精诱导的氧化应激Figure3.5.DepletionofmiR-29bexacerbatesoxidativestressafterchronic-plus-bingeethanolfeeding.(A)Imm....



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