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| 1 | Pathogenesis and management issues for non-alcoholic fatty liver disease显示文摘Nonalcoholic fatty liver disease (NAFLD) has, although it is a very common disorder, only relatively recently gained broader interest among physicians and scientists. Fatty liver has been documented in up to 10 to 15 percent of normal individuals and 70 to 80 percent of obese individuals. Although the pathophysiology of NAFLD is still subject to intensive research, several players and mechanisms have been suggested based on the substantial evidence. Excessive hepatocyte triglyceride accumulation resulting from insulin resistance is the first step in the proposed 'two hit' model of the pathogenesis of NAFLD. Oxidative stress resulting from mitochondrial fatty acids oxidation, NF-κB-dependent inflammatory cytokine expression and adipocytokines are all considered to be the potential factors causing second hits which lead to hepatocyte injury, inflammation and fibrosis. Although it was initially believed that NAFLD is a completely benign disorder, histologic follow-up studies have showed that fibrosis progression occurs in about a third of patients. A small number of patients with NAFLD eventually ends up with end-stage liver disease and even hepatocellular carcinoma. Although liver biopsy is currently the only way to confirm the NAFLD diagnosis and distinguish between fatty liver alone and NASH, no guidelines or firm recommendations can still be made as for when and in whom it is necessary. Increased physical activity, gradual weight reduction and in selected cases bariatric surgery remain the mainstay of NAFLD therapy. Studies with pharmacologic agents are showing promising results, but available data are still insufficient to make specific recommendations; their use therefore remains highly individual. | Marko Duvnjak Ivan Leroti Neven Bari Vedran Tomai Lucija Virovi Juki Vedran Velagi | 2007 | World Journal of Gastroenterology2007，13，34： | 74 |
| 2 | Non-alcoholic fatty liver disease: What the clinician needs to know显示文摘Non-alcoholic fatty liver disease(NAFLD) is the most frequent cause of liver disease in the Western world. Furthermore, it is increasing worldwide, paralleling the obesity pandemic. Though highly frequent, only about one fifth of affected subjects are at risk of developing the progressive form of the disease, non-alcoholic steatohepatitis with fibrosis. Even in the latter, liver disease is slowly progressive, though, since it is so prevalent, it is already the third cause of liver transplantation in the United States, and it is predicted to get to the top of the ranking in few years. Of relevance, fatty liver is also associated with increased overall mortality and particularly increased cardiovascular mortality. The literature and amount of published papers on NAFLD is increasing as fast as its prevalence, which makes it difficult to keep updated in this topic. This review aims to summarize the latest knowledge on NAFLD, in order to help clinicians understanding its pathogenesis and advances on diagnosis and treatment. | Mariana Verdelho Machado Helena Cortez-Pinto | 2014 | World Journal of Gastroenterology2014，20，36： | 45 |
| 3 | 肝星状细胞激活与信号转导显示文摘肝纤维化是多种慢性肝病向肝硬化发展的必经阶段,是所有慢性肝病的共同病理基础.目前认为肝星状细胞的激活是肝纤维化形成的关键,各种致病因素作用下引起肝损伤,释放多种细胞因子,如转化生长因子β、血管紧张素、瘦素,通过各种信号转导使肝星状细胞激活.本文就肝星状细胞激活过程中一些重要的膜受体、核受体信号转导途径及其研究进展作一综述. | 申月明 朱萱 | 2007 | 世界华人消化杂志2007，15，8： | 5 |
| 4 | 非酒精性脂肪性肝病的诊疗进展显示文摘随着肥胖和代谢综合征在全球流行,非酒精性脂肪性肝病(NAFLD)增长迅速,近年来新的诊断方法,特别是影像学等无创性诊断方法不断提出,为NAFLD的临床提供了很大帮助,但仍然不能取代肝活检在其诊断中的重要地位;同时NAFLD的治疗也有很大进展,在改变生活方式的基础上包括胰岛素增敏剂、降脂药、血管紧张素转换酶抑制剂等药物的应用,为NAFLD的治疗提供了新的方法,但其疗效仍需要进一步的临床观察。 | 张颖 张志广 | 2010 | 医学综述2010，16，24： | 4 |
| 5 | 血管紧张素Ⅱ对肝星状细胞迁移和增殖的影响显示文摘目的:探讨血管紧张素Ⅱ(ANGⅡ)对肝星状细胞(HSC)增殖、迁移活性的影响.方法:体外培养HSC,在不同浓度的ANGⅡ作用下,观察HSCs生长情况并绘制生长曲线,采用MTT法测定细胞增殖、Transwell小室检测细胞迁移.结果:1,2,4,8,10 umol/L ANGⅡ可显著促进HSC增殖,与空白对照组相比有显著差异(F= 2.305,P<0.05;F=4.003,6.833,8.855,21.066,P<0.01).随作用浓度的增加,细胞增殖活性显著提高,相关分析显示呈正相关(r=0.917,P<0.01).10,8,4μmol/L的ANGⅡ可显著诱导HSC迁移,与空白对照组相比差异显著(F= 22.084,15.155,10.392,P<0.01).随ANGⅡ浓度的增加,细胞迁移率显著升高,相关分析显示呈正相关(r=0.952,P<0.01).结论:ANGⅡ可显著诱导HSC增殖与迁移,并随剂量的增加作用加强. | 杨玲 朱清静 侯晓华 胡胜军 徐敏 朱锐 | 2007 | 世界华人消化杂志2007，15，9： | 4 |
| 6 | 肾素-血管紧张素系统阻断剂治疗代谢综合征的进展显示文摘代谢综合征以胰岛素抵抗为主要特征,是心血管疾病的危险因素。非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)是代谢综合征在肝脏的表现。肾素-血管紧张素系统(renin-angiotensin system,RAS)的激活参与了代谢综合征的发生、发展,阻断RAS的激活是代谢综合征的治疗途径之一。RAS阻断剂包括血管紧张素转换酶抑制剂(angiotensin converting enzyme inhibitor,ACEI)和血管紧张素Ⅱ受体拮抗剂(angiotensin receptor blockade,ARB),可降低血压、改善胰岛β细胞功能和胰岛素抵抗,但RAS阻断剂对NAFLD的疗效尚存在争议。该文就RAS阻断剂治疗代谢综合征的进展进行了综述。 | 张凤 周华梅 张霞 | 2012 | 中国药业2012，21，6： | 3 |
| 7 | 肝组织肾素-血管紧张素-醛固酮系统与肝纤维化的关系显示文摘慢性肝损伤过程中常伴有肝组织局部肾素-血管紧张素-醛固酮系统(RAAS)的激活,RAAS激活后产生的局部组织血管紧张素-Ⅱ(AngⅡ)和醛固酮是促进肝纤维化形成的两大重要因素,在肝纤维化的治疗中有效的阻止RAAS系统可以改善预后。 | 张敏 吴万春 | 2009 | 国际消化病杂志2009，29，1： | 3 |
| 8 | 非酒精性脂肪性肝炎的诊断和治疗进展显示文摘 | 魏爽 沈镭 陆伦根 | 2008 | 上海医学2008，31，11： | 2 |
| 9 | 肾素血管紧张素系统在非酒精性脂肪性肝病发病机制中的实验研究显示文摘目的探讨肝组织肾素血管紧张素系统在非酒精性脂肪性肝病(NAFLD)发病机制中的作用。方法取Wistar大鼠24只均分为模型组和对照组。对照组予正常饮食,模型组予高脂饮食,8周后处死大鼠,测定血清肝功能、血脂、血糖和胰岛素,分别以HE染色和苦味酸一天狼星红染色进行肝组织病理学观察,ELISA法测定肝组织血管紧张素Ⅱ(AngII)浓度,免疫组织化学法测定肝组织转化生长因子(TGF)-β1表达水平。结果模型组大鼠高脂喂养8周后,体质量、肝指数、肝功能、血脂、血胰岛素显著高于对照组[体质量:(463.50±22.72)g比(405.12±10.32)g;肝指数:(3.75±0.21)比(2.66±0.15);ALT:(79.8±8.6)U/L比(58.8±11.6)U/L;AST:(200.01士51.72)U/L比(150.30±37.27)U/L;胆固醇:(3.67±0.48)mmol/L比(1.50±0.23)mmol/L;三酰甘油:(2.06±0.40)mmol/L比(O.71±0.34)mmol/L;胰岛素:(17.37±2.89)pmol/L比(11.08±2.12)pmol/L],差异均有统计学意义(均P〈0.01)。模型组大鼠病理组织学均出现明显的肝脂肪变性,且部分出现小叶内和汇管区炎性反应,部分肝组织出现明显的纤维化改变。模型组大鼠肝组织AngII[(32.80±2.81)pg/ml]较对照组[(22.83土1.75)pg/m1]高(t=9.559,P〈O.01)。免疫组织化学检测显示模型组TGF[31表达量明显高于对照组(Z=-2.540,P=0.011)。Spearman相关性分析显示,大鼠肝组织内AngⅡ浓度增加程度与肝脂肪变积分(r=0.644,P=0.002)和TGF-131表达量(r=0.470,P=0.037)均呈正相关。结论AngⅡ和TGF-β1在NAFLD模型大鼠的肝组织内浓度明显增加,肾素血管紧张素系统可能参与了NAFLD的发生和发展。 | 胡晓娜 史冬梅 刘方 高占娟 马海芬 黄一沁 尹曙明 保志军 | 2012 | 中华消化杂志2012，32，6： | 2 |
| 10 | 非酒精性脂肪性肝病发病机制的研究进展显示文摘 | 谭德安 府伟灵 | 2007 | 医学临床研究2007，24，7： | 1 |
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