【摘要】：目的：通過(guò)測(cè)定非酒精性脂肪性肝炎(NASH)肝臟組織切片中CD14、NALP3、Caspase-1的表達(dá),探討激活NALP3炎性小體的內(nèi)毒素病原相關(guān)分子模式在NASH患者肝臟炎癥發(fā)生及發(fā)展中的可能作用。 方法：收集中南大學(xué)湘雅二醫(yī)院經(jīng)病理證實(shí)為非酒精性脂肪肝的住院病人的肝組織蠟塊標(biāo)本26例,按脂肪性肝炎和單純性脂肪肝區(qū)分標(biāo)準(zhǔn)分為脂肪性肝炎組即NASH組(n=12)和單純性脂肪肝組即NAFL組(n=14),取經(jīng)病理證實(shí)為正常的肝臟組織為正常對(duì)照組即NC組(n=10)。三組病例均從病例資料中統(tǒng)計(jì)其性別(S)、年齡(A)、體質(zhì)指數(shù)(BMI)、收縮壓(SBP)、舒張壓(DBP)、甘油三酯(TG)、空腹血糖(FBG)、丙氨酸氨基轉(zhuǎn)移酶(ALT)、門冬氨酸氨基轉(zhuǎn)移酶(AST)。對(duì)三組肝組織標(biāo)本的炎癥活動(dòng)程度及纖維化程度進(jìn)行評(píng)分。CD14、NALP3、Caspase-1測(cè)定采用免疫組織化學(xué)技術(shù)(immunohistochemistry, IHC)。應(yīng)用SPSS17.0統(tǒng)計(jì)軟件進(jìn)行數(shù)據(jù)處理,計(jì)數(shù)資料采用x2或fisher方法,計(jì)量資料采用獨(dú)立樣本之間T檢驗(yàn),關(guān)系判定采用pearson相關(guān)分析和logistic回歸分析,以P0.05為具有統(tǒng)計(jì)學(xué)意義、P0.01具有顯著性。 結(jié)果：臨床實(shí)驗(yàn)室資料比較除年齡、性別外,體質(zhì)指數(shù)(BMI)、收縮壓(SBP)、舒張壓(DBP)、甘油三酯(TG)、空腹血糖(FBG)、丙氨酸氨基轉(zhuǎn)移酶(ALT)、門冬氨酸氨基轉(zhuǎn)移酶(AST)等其余各項(xiàng)因素均存在統(tǒng)計(jì)學(xué)差異(P0.05)。在所選病例中以脂肪性肝炎有無(wú)(無(wú)脂肪性肝炎為0,有脂肪性肝炎為1)為因變量,各相關(guān)因素為自變量進(jìn)行Logistic回歸分析,結(jié)果顯示體質(zhì)指數(shù)、空腹血糖、甘油三酯、血壓是發(fā)生脂肪性肝炎的主要影響因素。 對(duì)各組CD14、NALP3、Caspase-1的含量進(jìn)行半定量分析,結(jié)果表明NASH組各指標(biāo)含量較NAFL組及NC組明顯增高,差異有統(tǒng)計(jì)學(xué)意義。并且各觀察指標(biāo)的含量、炎癥活動(dòng)程度及纖維化程度之間呈正相關(guān)。 結(jié)論：(一)肥胖、高血糖、高脂血癥、高血壓等是NASH發(fā)生的主要影響因素。 (二)內(nèi)毒素作為病原相關(guān)分子模式信號(hào)通過(guò)激活NALP3炎性體,導(dǎo)致肝臟炎癥,可能是促進(jìn)NASH發(fā)生和進(jìn)展的機(jī)制之一。
[Abstract]:Aim: to investigate the possible role of endotoxin-associated molecular model of activating NALP3 inflammatory corpuscles in the occurrence and development of liver inflammation in patients with NASH by detecting the expression of CD14,NALP3,Caspase-1 in liver sections of (NASH) patients with non-alcoholic steatohepatitis. Methods: a total of 26 samples of paraffin tissue from patients with non-alcoholic fatty liver confirmed by pathology in Xiangya second Hospital of Central South University were collected. According to the criteria of differentiating fatty hepatitis from simple fatty liver, they were divided into two groups: NASH group (n = 12) and simple fatty liver group (n ~ (14). The normal liver tissue proved to be normal by pathology was normal control group (n ~ (10). Three groups of patients were counted from the data of their sex (S), age (A), body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), triglyceride (TG), fasting blood glucose (FBG), alanine aminotransferase (ALT), aspartate aminotransferase (AST). The degree of inflammatory activity and fibrosis in three groups of liver tissue specimens were evaluated. CD14 NALP3Caspase-1 was determined by immunohistochemical technique (immunohistochemistry, IHC). The data were processed by SPSS17.0 statistical software. The counting data were analyzed by X2 or fisher method, the measurement data were measured by T test among independent samples, and the relationship was determined by pearson correlation analysis and logistic regression analysis. Results: in addition to age and sex, the clinical laboratory data were compared. Body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), triglyceride (TG), fasting blood glucose (FBG), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and other factors were statistically different (P0.05). In the selected cases, whether there was fatty hepatitis (0 for non-fat hepatitis and 1 for fatty hepatitis) was used as dependent variable, and the correlation factors were independent variables for Logistic regression analysis. The results showed that body mass index, fasting blood glucose, triglyceride were the main factors. Blood pressure is the main influencing factor of fatty hepatitis. The results showed that the content of CD14,NALP3,Caspase-1 in NASH group was significantly higher than that in NAFL group and NC group, and the difference was statistically significant. There was a positive correlation between the content of the observed indexes, the degree of inflammatory activity and the degree of fibrosis. Conclusion: (1) Obesity, hyperglycemia, hyperlipidemia and hypertension are the main influencing factors of NASH. (2) Endotoxin, as a signal of pathogen-associated molecular model, may be one of the mechanisms of promoting the pathogenesis and progression of NALP3 by activating the inflammatory body of NASH and leading to hepatic inflammation.
【學(xué)位授予單位】：中南大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R575.1

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