1、安徽医科大学硕士学位论文中 英 文 缩 写 对 照 表缩写中文名称英文名称ALT谷丙转氨酶alanine aminotransferaseArg-1FBG增强精氨酸酶-1 空腹血糖arginase-1fasting blood glucose52FINSFizz1 FFA HFHSjHIV IL-1 IL-4 IL-6 IL-10 IL-12 IL-13 IR KCMCP-1 M1 M2NAFLD NCNF-kB空腹血浆胰岛素类抵抗素 游离脂肪酸高脂组高脂复合日本血吸虫感染组人类免疫缺陷病毒白细胞介素-1白细胞介素-4白细胞介素-6 白细胞介素-10 白细胞介素-12 白细胞介素-13 胰岛素
2、抵抗 库普弗细胞单核细胞趋化蛋白-l 经典活化型巨噬细胞选择活化型巨噬细胞非酒精性脂肪肝病 正常对照组核因子- kappa Bfasting plasma insulin resistin-like-free fatty acids high-fat grouphigh-fat with schistosoma japonicum infected groupHuman Immunodeficiency VirusInterleukin-1 Interleukin-4 Interleukin-6 Interleukin-10 Interleukin-12 Interleukin-13 insu
3、lin resistance Kupffer cellsmonocyte chemoattractant protein-1 classically activated macrophages alternatively activated macrophages non-alcoholic fatty liver disease normal control groupnuclear factor kappa B安徽医科大学硕士学位论文RT-RCR逆转录-聚合酶链反应reverse transcription-polymerasechain reactionSJ日本血吸虫schistosom
4、a japonicumTG甘油三酯triglycerideTC胆固醇cholesterolTNF-肿瘤坏死因子-tumor necrosis factor-STZ链脲佐菌素StreptozotocinTh II 型辅助 T 细胞T helper cells ITh IIII 型辅助 T 细胞T helper cells IIT1DM1 型糖尿病type 1 diabetes mellitusT2DM2 型糖尿病type 2 diabetes mellitusYm1类几丁质酶 3 样分子chitinase 3-like 3日本血吸虫感染对饮食诱导的 C57BL/6J 脂肪肝小鼠肝组织 TNF-,
5、 NF-kB 及 Ym-1 mRNA 表达的影响中文摘要目的 观察日本血吸虫感染对高脂饮食诱导的 C57BL/6J 脂肪肝小鼠肝脏组织结构与功能、肿瘤坏死因子-(tumor necrosis factor-, TNF-)、核因子-kB(nuclear factor kappa B, NF-kB)及巨噬细胞选择性活化标志物 Ym-1 mRNA 水平在肝脏组织中表达的影响,探讨血吸虫感染后巨噬细胞选择性活化对肥胖小鼠肝脏及胰岛素抵抗的影响及可能机制。方法 36只雄性C57BL/6J小鼠, 随机分为正常对照(NC, n=12)组、高脂饮食(HF,n=12)组及高脂饮食复合日本血吸虫感染(HSj,n=
6、12)组。HF组经高脂饮食建立肥胖模型,HSj组经高脂饮食及日本血吸虫感染建立肥胖复合血吸虫感染模型。分别于高脂喂养第6 周末及12 周末时检测空腹血糖 ( fasting peripheral bloodglucose,FBG)、空腹血浆胰岛素(fasting plasma insulin,FINS)水平,并计算胰岛素抵抗指数(insulin resistance index,HOMA-IR),检测肝组织匀浆谷丙转氨酶( alanine aminotransferase , ALT )、甘油三酯( triglyceride , TG) 及胆固醇(cholesterol,TC)水平;HE染色观
7、察肝组织病理改变,逆转录-聚合酶链反应(reverse transcription polymerase chain reaction,RT-RCR)检测肝脏组织TNF-和NF-kB及M2型巨噬细胞的特异性标志物Ym-1 mRNA表达情况。结果1. 高脂喂养第6周末时,HF组及HSj组小鼠体重均较NC组增加20%,肥胖模型造模成功。第12周末时,HF组体重较NC组增加,具有统计学意义(P0.05),HSj组体重与NC组比较无统计学意义,但低于HF组(P0.05)。2. 第6周末时HF组FINS、HOMA-IR较NC组升高,具有统计学意义(P0.05),HF组FBG较NC组升高差异无统计学意义,
8、HSj组HOMA-IR较HF组显著下降(P0.05),而HSj组FBG、FINS与HF组比较差异无统计学意义。第12周末时HF组FBG、FINS、HOMA-IR均进一步升高且明显高于同期NC组(P0.05),HSj组FBG、FINS、HOMA-IR均较同期HF组下降(P0.05)。3. 第6周末HF组小鼠肝匀浆TG较NC组升高有统计学意义(P0.05), TC及ALT含量与NC组比较无统计学差异。HSj组TC、TG水平较HF组下降(P0.05),ALT变化不明显。12周末时HF组肝匀浆TC、TG、ALT进一步较NC组升高(P0.05),HSj组TC、TG较同期HF组下降有统计学意义(P0.05
9、),但ALT升高(P0.05)。4. 肉眼观,在第6周末时,NC组小鼠肝脏红润,HF组小鼠肝脏边缘变钝、微黄色, 可见黄色脂肪斑,HSj组小鼠肝脏呈红褐色,体积较HF组肝脏小,可见颗粒状结节;第12周末时,NC组小鼠肝脏外观无明显异常,HF组及HSj组小鼠肝脏上述表现更加明显。5. 光学显微镜下,在第6周末和第12周末NC组小鼠肝组织HE染色均未见明显异常。第6周末时HF组小鼠肝细胞内可见大小不等的脂滴空泡,第12周末肝细胞内脂滴空泡更加明显,可见气球样变及纤维化,HSj组小鼠第6周末可见少量大小不等的脂滴空泡及肝细胞坏死,第12周末时肝细胞坏死和肝纤维化加重。第6周末及第12周末HF组肝小叶
10、内及汇管区均可见炎性细胞浸润,较同期HSj组浸润增多。6. RT-PCR在第6周和第12周末时检测HF组TNF- mRNA及NF-kB mRNA表达均高于HSj组和NC组(P0.05)。第6周末时,HF组Ym-1 mRNA的表达高于NC组和HSj组(P0.05),第12周末时HSj组Ym-1 mRNA表达强度高于HF组和NC组(P0.05),且较6周时表达增强(P0.05)。7. HF组小鼠HOMA-IR与肝组织TNF- mRNA光密度相对值呈正相关(P0.05);HSj组小鼠HOMA-IR与肝组织Ym-1mRNA光密度相对值呈负相关(P0.05)。结论1. 高脂饮食可诱导C57BL/6J肥胖
11、小鼠及脂肪肝模型的建立,该模型具有胰岛素抵抗的特征。2. 肥胖小鼠脂肪肝组织中炎症因子TNF-及调控因子NF-kB的表达水平与胰岛素抵抗的形成有一定的关系。3. 日本血吸虫感染可以增强肥胖小鼠脂肪肝肝组织中M2型巨噬细胞选择性表达水平,降低脂肪肝组织中TNF-及NF-kB水平的表达,减轻肝脏的脂肪变性及炎性细胞的浸润,改善胰岛素抵抗,其可能的机制与M2型巨噬细胞活化时抑制M1型巨噬细胞的促炎效应有关,但可能加重肝细胞坏死及肝纤维化。关键词 脂肪肝;炎症因子;胰岛素抵抗Effects of schistosoma japonicum infection on TNF-, NF-kB and Ym
12、-1 in diet-induced fatty liver of C57BL/6J miceAbstractObjective To observe the pathological structure, biochemical indicators, and changes of tumor necrosis factor-(TNF-), nuclear factor-kappa B (NF-kB) and macrophage M2 marker, specifically Ym-1, and explore the relationship and mechanism ofmacrop
13、hage polarization and insulin resistance in diet-induced obese and schistosoma japonicum infected C57BL/6J miceMethods 36 male C57BL/6J mice were randomly assigned into 3 groups: normal control (NC, n=12) group, high-fat diet (HF, n=12) group and high-fat diet with schistosoma japonicum infected (HS
14、j, n=12) group. They were fed with basic diet, high-fat diet group, respectively, and HSj group were infected schistosoma japonicum. Specimen was collected 6 and 12 weeks after high-fat diet, separately. The levels of fasting blood glucose (FBG), fasting plasma insulin (FINS) and insulin (HOMA-IR) w
15、ere detected and the contents of liver homogenate alanine aminotransferase (ALT) , triglyceride (TG) and cholesterol (TC) were measured. The pathological changes of liver were observed by HE staining. TNF-, NF-kB and Ym-1 mRNA were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).Results1. When having been fed for 6 weeks, the weight of HF and HSj group increased 20% than the NC group, and obesity model mice w
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