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| 1 | 酒精性肝病发病机制的研究进展显示文摘酒精性肝病(alcoholicliverdisease,ALD)是长期大量饮酒导致的肝脏损伤性疾病。在世界范围内是导致肝脏慢性损伤的主要疾病,ALD包括轻症酒精性肝病(mildalcoholicinjury,MAI)、酒精性脂肪肝(alcoholicfattyliver,AFL)、酒精性肝炎(alcoholichepatitis,AH)、酒精性肝纤维化(alcoholichepaticfibrosis,AHF)、酒精性肝硬化(alcoholiccirrhosis.AC)5个阶段。 | 邬升 郑世华 仝巧云 | 2013 | 实用医学杂志2013，29，12： | 19 |
| 2 | Ethanol and liver: Recent insights into the mechanisms of ethanol-induced fatty liver显示文摘Alcoholic fatty liver disease(AFLD),a potentially pathologic condition,can progress to steatohepatitis,fibrosis,and cirrhosis,leading to an increased probability of hepatic failure and death.Alcohol induces fatty liver by increasing the ratio of reduced form of nicotinamide adenine dinucleotide to oxidized form of nicotinamide adenine dinucleotide in hepatocytes;increasing hepatic sterol regulatory element-binding protein(SREBP)-1,plasminogen activator inhibitor(PAI)-1,and early growth response-1 activity;and decreasing hepatic peroxisome proliferator-activated receptor-αactivity.Alcohol activates the innate immune system and induces an imbalance of the immune response,which is followed by activated Kupffer cell-derived tumor necrosis factor(TNF)-αoverproduction,which is in turn responsible for the changes in the hepatic SREBP-1 and PAI-1 activity.Alcohol abuse promotes the migration of bone marrowderived cells(BMDCs)to the liver and then reprograms TNF-αexpression from BMDCs.Chronic alcohol intake triggers the sympathetic hyperactivity-activated hepatic stellate cell(HSC)feedback loop that in turn activates the HSCs,resulting in HSC-derived TNF-αoverproduction.Carvedilol may block this feedback loop by suppressing sympathetic activity,which attenuates the progression of AFLD.Clinical studies evaluating com-bination therapy of carvedilol with a TNF-αinhibitor to treat patients with AFLD are warranted to prevent the development of alcoholic liver disease. | Jinyao Liu | 2014 | World Journal of Gastroenterology2014，20，40： | 16 |
| 3 | New advances in molecular mechanisms and emerging therapeutic targets in alcoholic liver diseases显示文摘Alcoholic liver disease is a major health problem in the United States and worldwide. Chronic alcohol consumption can cause steatosis, inflammation, fibrosis, cirrhosis and even liver cancer. Significant progress has been made to understand key events and molecular players for the onset and progression of alcoholic liver disease from both experimental and clinical alcohol studies. No successful treatments are currently available for treating alcoholic liver disease; therefore, development of novel pathophysiological-targeted therapies is urgently needed. This review summarizes the recent progress on animal models used to study alcoholic liver disease and the detrimental factors that contribute to alcoholic liver disease pathogenesis including miRNAs, S-adenosylmethionine, Zinc deficiency, cytosolic lipin-1β, IRF3-mediated apoptosis, RIP3-mediated necrosis and hepcidin. In addition, we summarize emerging adaptive protective effects induced by alcohol to attenuate alcohol-induced liver pathogenesis including FoxO3, IL-22, autophagy and nuclear lipin-1α. | Jessica A Williams Sharon Manley Wen-Xing Ding | 2014 | World Journal of Gastroenterology2014，20，36： | 10 |
| 4 | New treatment options for alcoholic hepatitis显示文摘The burden of alcoholic liver disease has rapidly grown in the past two decades and is expected to increase further in the coming years. Alcoholic hepatitis, the most florid presentation of alcoholic liver disease, continues to have high morbidity and mortality, with significant financial and healthcare burden with limited treatment options. Steroids remain the current standard of care in severe alcoholic hepatitis in carefully selected patients. No specific treatments are available for those patients who are steroid ineligible, intolerant or unresponsive. Liver transplant has shown good short-term outcome; however, feasibility, ethical and economic concerns remain. Modification of gut microbiota composition and their products, such as lipopolysaccharide, nutritional interventions, immune modulation, increasing steroid sensitivity, genetic polymorphism and epigenetic modification of alcohol induced liver damage, augmenting hepatic regeneration using GCSF are potential therapeutic avenues in steroid non-responsive/ineligible patients. With better understanding of the pathophysiology, using 'Omics' platforms, newer options for patients with alcoholic hepatitis are expected soon. | Saggere Muralikrishna Shasthry Shiv Kumar Sarin | 2016 | World Journal of Gastroenterology2016，22，15： | 5 |
| 5 | 赶黄草配伍葛花对乙醇诱导下L-02肝细胞的影响显示文摘目的:探究赶黄草配伍葛花制备的含药血清对乙醇诱导的L-02肝细胞的影响及其可能机制。方法:分别制备不同配比含药血清后,将L-02肝细胞分为6组进行实验:空白对照组,模型组,赶黄草配伍葛花1∶1组、2∶1组和1∶2组,凯希莱组。MTT法检测含药血清对乙醇诱导的L-02细胞存活率的影响;酶标法检测培养液中丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)及受损细胞中超氧化物歧化酶(SOD)和丙二醛(MDA)的水平;realtime PCR法和Western blot检测赶黄草配伍葛花对L-02肝细胞中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、核因子E2相关因子2(Nrf2)和血红素加氧酶1(HO-1)mRNA及蛋白表达的影响。结果:与空白对照组相比,模型组ALT、AST及MDA水平明显升高,SOD活性明显降低(P<0.01);与模型组相比,各药物组ALT、AST及MDA水平明显降低,SOD活性明显升高(P<0.01)。机理研究中,与空白对照组相比,模型组TNF-α和IL-6的mRNA和蛋白表达显著升高,Nrf2和HO-1的mRNA和蛋白表达显著降低(P<0.01);与模型组相比,各配伍组TNF-α和IL-6的mRNA和蛋白表达显著降低,Nrf2和HO-1的mRNA和蛋白表达显著升高(P<0.01)。结论:赶黄草配伍葛花含药血清可能通过下调TNF-α和IL-6的表达,上调Nrf2和HO-1的表达,从而降低L-02肝细胞的炎症反应并减轻氧化应激,进而发挥治疗酒精性肝损伤的作用。 | 舒承倩 吴晶魁 周滢 | 2018 | 中国病理生理杂志2018，34，6： | 5 |
| 6 | 酒精性肝病的自身免疫特征及免疫调节治疗显示文摘酒精性肝病的发病机制尚不十分清楚。患者循环中存在乙醇代谢产物与某些蛋白成分结合后形成的加合物,存在非特异性自身抗体,存在Mallory小体、肝特异性脂蛋白(LSP)、肝细胞膜抗原(LMA)等多种抗原,存在抗体与可溶性抗原结合而形成的免疫复合物及多种细胞因子等现象,均提示自身免疫耐受的破坏是酒精性肝病发生的始动因素。对酒精性肝病免疫发病机制的深入探讨有助于推动治疗技术的发展进步。 | 王眭 亓文骞 赵平 王江滨 | 2012 | 国际消化病杂志2012，32，6： | 3 |
| 7 | 哈蟆油蛋白酶解物对乙醇诱导的L-02细胞损伤的作用显示文摘目的:研究哈蟆油蛋白酶解物(ORPH)对乙醇诱导的L-02细胞损伤相关通路蛋白表达影响的作用机制研究。方法:复合酶解法制备ORPH,以400 mmol·L^(-1)乙醇建立L-02肝细胞损伤模型,细胞增殖与活性检测试剂盒-8(CCK-8)检测细胞活力;流式细胞术检测细胞凋亡、周期变化,JC-1/Hochest染色观察形态学变化;蛋白免疫印迹法(Western blot)检测凋亡相关蛋白、丝裂原活化蛋白激酶(MAPK)信号通路及细胞焦亡相关蛋白在L-02肝细胞中的表达变化,研究ORPH对乙醇所致肝细胞损伤的保护作用及机制。结果:CCK-8法结果表明400 mmol·L^(-1)乙醇可在12 h内明显引起L-02肝细胞损伤;与空白组比较,模型组L-02细胞活力显著下降(P<0.01),细胞处于G0/G1期的细胞占比显著升高(P<0.01),细胞总凋亡率显著升高(P<0.01),线粒体膜电位下降;B细胞淋巴瘤-2(Bcl-2)相关X蛋白(Bax),细胞色素C(Cyt C),半胱氨酸天冬氨酸蛋白水解酶-3(Caspase-3)凋亡相关蛋白的表达明显升高(P<0.05,P<0.01),MAPK信号通路相关蛋白c-Jun氨基末端激酶(JNK),p38丝裂原活化蛋白激酶(p38 MAPK)明显上调(P<0.05,P<0.01),且焦亡蛋白Caspase-1,白细胞介素-1β(IL^(-1)β)表达明显增强(P<0.05),Bcl-2显著下降(P<0.01);与模型组比较,ORPH处理组细胞周期阻滞有所改善(P<0.05,P<0.01),细胞总凋亡率显著下降(P<0.01),线粒体膜电位升高,呈剂量相关性;Bax,Cyt C,Caspase-3蛋白表达明显降低(P<0.05,P<0.01),Bcl-2蛋白表达升高(P<0.05,P<0.01),MAPK信号通路相关蛋白及焦亡相关蛋白表达均呈下降趋势(P<0.05,P<0.01)。结论:ORPH可通过抑制乙醇诱导L-02肝细胞引起的氧化应激肝细胞损伤,改善恢复线粒体膜电位,降低线粒体介导的细胞凋亡通路蛋白的表达,并抑制MAPK信号通路相关蛋白、焦亡通路相关蛋白表达,从而降低乙醇诱导L-02肝细胞的线粒体功能障碍及炎症反应并减轻氧化应激,对酒精性肝损伤起到治疗作用。 | 张怡 郑冉 于奇 焦丽丽 李波 刘达 李宜平 | 2021 | 中国实验方剂学杂志2021，27，15： | 2 |
| 8 | Focus on alcoholic liver disease:From nosography to treatment显示文摘Abusive alcohol intake currently ranks as a major cause of liver disease, and is associated with significant mortality worldwide. Alcoholic liver disease(ALD) generically defines liver abnormalities ranging from liver steatosis to the end-stages of disease such as liver cirrhosis. Information regarding the precise incidence and prevalence of ALD is still limited by a lack of large population-based studies and by the absence of large systematic reviews of all epidemiological data available. However, existing collected data show an overall increase in the number of alcohol abusers and alcoholrelated liver disease. The burden exerted on medical systems worldwide is significant, with hospitalization and management costs rising constantly over the years. A great number of all cirrhosis-related deaths in Europe and a significant percentage worldwide areassociated with alcohol consumption. The main possible risk factors for ALD are the amount and duration of alcohol abuse, patterns of drinking and the type of alcoholic beverage consumed. However, ALD does not progress to cirrhosis in all patients, therefore a series of additional factors are implicated. Even though insufficiently studied, genetic factors are generally regarded as highly important, and the presence of comorbidities and dietary habits seem to play a role in disease onset and progression. This lack of clear pathophysiological data further translates in the absence of definite treatment for ALD and shall prove challenging in the coming years. In this article, we aimed to briefly review epidemiologic data on the burden of ALD, risk factors, clinical and nosographic as well as therapeutic aspects of this disease. Without attempting to be exhaustive, this short topic highlight emphasizes each point and may serve as a general guidance tool in the complicated literature related to ALD. | Letitia Adela Maria Streba Cristin Constantin Vere Costin Teodor Streba Marius Eugen Ciurea | 2014 | World Journal of Gastroenterology2014，20，25： | 0 |
| 9 | 英夫利昔单抗治疗重症酒精性肝炎的系统评价显示文摘目的 评价英夫利昔单抗治疗重症酒精性肝炎(SAH)的临床疗效和安全性.方法 计算机检索PubMed、EMbase、Web of Science、OVID和Cochrane图书馆系统评价资料库、CBMdisc和中国期刊网全文数据库(CNKI)等电子数据库,检索时限为建库至2013年3月,以SAH、重症酒精性肝病、英夫利昔单抗、肿瘤坏死因子拮抗剂等名称作为关键词、主题词、自由词,查找英夫利昔单抗治疗SAH的随机对照试验(RCT),对符合纳入标准的临床研究进行Meta分析.结果 共纳入2篇RCT,56例SAH患者,采用英夫利昔单抗(10 mg/kg)联合糖皮质激素(40 mg/d)治疗SAH,可能因严重感染的高患病率而加速患者死亡,预后不良;采用英夫利昔单抗(5 mg/kg)联合糖皮质激素(40mg/d)治疗,具有良好的耐受性,患者的Maddrey评分显著改善.结论 现有的临床证据显示,英夫利昔单抗治疗SAH的疗效和安全性依据不足,需要更多大样本、不同剂量的RCT指导临床. | 田晓娟 郭元虎 李慧妍 | 2014 | 中国医师进修杂志2014，37，12： | 0 |
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