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| 1 | 非酒精性脂肪肝分子发病机制的研究进展显示文摘非酒精性脂肪性肝病(nonalcoholic fatty liver disease,NAFLD)是一种常见肝病,且发病率有逐年增加的趋势.本文概述近年来国内外学者在NAFLD发病机制方面的主要成果和观点,探讨在NAFLD发病中基因的作用,旨在阐明NAFLD发病的分子机制. | 钱林 胡小宣 | 2008 | 世界华人消化杂志2008，16，25： | 19 |
| 2 | 酒精性肝损伤研究及中药治疗进展显示文摘长期过量饮酒所致的酒精性肝损伤(ALI)严重影响人类健康,其主要是由酒精及其代谢产物对肝脏造成毒副作用。研究发现很多中药可缓解ALI,且具有疗效确切、不良反应小、多成分、多靶点、多环节整合作用等特点,已取得了较好临床效果。文章综述ALI发病机制及中药对其防治作用的研究进展,提出目前研究存在的一些问题并对未来研究方向进行展望。 | 董金材 王曦 李凤娇 曾鳞粞 顾雯 杨兴鑫 俞捷 | 2019 | 辽宁中医杂志2019，46，8： | 14 |
| 3 | CYP2E1调控酒精性肝病发病机制的研究进展显示文摘酒精性肝病(alcoholic liver disease,ALD)是长期饮酒或数周内大量酗酒引起的肝脏损伤,细胞色素P450 2E1(CYP2E1)是参与酒精代谢的主要酶类之一,在酒精毒性代谢和ALD致病过程中起着重要作用。CYP2E1体内表达量、活性水平、代谢酒精过程中产生的氧自由基量以及毒性代谢产物能够通过不同方式影响ALD的患病风险以及病程发展,其影响机制与多条信号通路有关。各信号通路间交互错杂,相互作用,共同调控机体的自我保护功能和ALD的形成及发展。本文将归纳总结CYP2E1调控ALD的形成及发展的保护和损伤机制等方面相关信号通路的研究进展,为今后ALD的防治研究提供帮助。 | 陈丹 林秀贤 陈尧 | 2017 | 中国临床药理学与治疗学2017，22，2： | 12 |
| 4 | 利用细菌/杆状病毒系统在昆虫细胞中表达人CYP2E1显示文摘目的:获得人CYP2E1重组酶,并用该重组酶的特征性探针底物对其进行代谢活性研究。方法:以人肝组织RNA为模板,通过RT-PCR得到CYP2E1 cDNA片断,然后与pFastBac质粒连接,得到pFastBac-CYP2E1重组质粒,将其转化E.coli DH 10Bac大肠杆菌,通过转座作用,获得重组Bacmid-CYP2E1,将其转染草地夜蛾细胞(Sf9)后,产生重组杆状病毒。将该病毒以及分别含有人CYPOR和人CYPb5的病毒共同感染Sf9细胞,收集共表达蛋白,以氯唑沙宗为底物鉴定重组酶的活性。结果:利用细菌/杆状病毒系统得到重组人CYP2E1的表达,其对氯唑沙宗的Km值为(72.4±8.7)μmol.L-1,Vmax值为(2.41±0.10)μmol.min-1.g-1蛋白。结论:利用杆状病毒系统成功表达了有催化活性的人CYP2E1重组酶,其活性与文献报道值相似。 | 路珂 曾苏 姚彤炜 | 2008 | 浙江大学学报(医学版)2008，37，2： | 4 |
| 5 | 细胞色素P450 2E1与酒精性肝病显示文摘细胞色素P4502E1(cytochrome P4502E1,CYP2E1)是细胞色素P450的乙醇诱导形式,在乙醇氧化酶途径中起重要作用。现通过查阅国内外相关文献综述了近年来关于CYP2E1在酒精性肝病方面的研究进展。 | 朱海珍 魏文树 | 2008 | 海峡药学2008，20，10： | 4 |
| 6 | 细胞色素P4502E1酶与非酒精性脂肪肝的关系显示文摘目的:探讨细胞色素P4502E1(CYP2E1)酶基因多态性与非酒精性脂肪性肝病(NAFLD)的关系及NAFLD的遗传学发病机制.方法:采用聚合酶链反应——限制性片段长度多态性分析法(PCR-RFLP)对40例非酒精性脂肪肝患者,20例酒精性肝病患者,20例非脂肪肝对照者,20例正常对照者分析CYP2E1基因多态性,并进行相关性分析.结果:NAFLD中c2等位基因型与正常对照组(x^2=8.376,P=0.004)和非脂肪肝对照组(x^2= 6.769,P=0.005)相比明显升高,差异有统计学意义(P<0.01),NAFLD中基因型分布与酒精性肝病相比无明显改变,差异无统计学意义(P =0.896).在NAFLD中肝脏病变程度不同,c2等位基因频率不同,在脂肪性肝炎(P=0.04)和肝硬化(P=0.000)中,差异有统计学意义(P<0.05).结论:NAFLD与CYP2E1酶基因多态性有关,同时也为研究NAFLD遗传易感性提供了新的思路. | 郭艳梅 王沁 祁志 | 2007 | 世界华人消化杂志2007，15，16： | 2 |
| 7 | Three new alternative splicing variants of human cytochrome P450 2D6 mRNA in human extratumoral liver tissue显示文摘AIM: To identify the new alternative splicing variants of human CYP2D6 in human extratumoral liver tissue with RT-PCR and sequencing. METHODS: Full length of human CYP2D6 cDNAs was amplificated by reverse transcription-polymerase chain reaction (RT-PCR) from a human extratumoral liver tissue and cloned into pGEM-T vector. The cDNA was sequenced. Exons from 1 to 4 of human CYP2D6 cDNAs were also amplificated by RT-PCR from extratumoral liver tissues of 17 human hepatocellular carcinomas. Some RT-PCR products were sequenced. Exons 1 to 4 of CYP2D6 gene were amplified by PCR from extratumoral liver tissue DNA. Two PCR products from extratumoral liver tissues expressing skipped mRNA were partially sequenced. RESULTS: One of the CYP2D6 cDNAs had 470 nucleotides from 79 to 548 (3′ portion of exons i to 5′ portion of exon 4), and was skipped. Exons 1 to 4 of CYP2D6 cDNA were assayed with RT-PCR in 17 extratumoral liver tissues. Both wild type and skipped mRNAs were expressed in 4 samples, only wild type mRNA was expressed in 5 samples, and only skipped mRNA was expressed in 8 samples. Two more variants were identified by sequencing the RT-PCR products of exons 1 to 4 of CYP2D6 cDNA. The second variant skipped 411 nucleotides from 175 to 585. This variant was identified in 4 different liver tissues by sequencing the RT-PCR products. We sequenced partially 2 of the PCR products amplified of CYP2D6 exon 1 to exon 4 from extratumoral liver tissue genomic DNA that only expressed skipped mRNA by RT-PCR. No point mutations around exon 1, intron 1, and exon 4, and no deletion in CYP2D6 gene were detected. The third variant was the skipped exon 3, and 153bp was lost. CONCLUSION: Three new alternative splicing variants of CYP2D6 mRNA have been identified. They may not be caused by gene mutation and may lose CYP2D6 activity and act as a down-regulator of CYP2D6. | JianZhuge Ying-NianYu | 2004 | World Journal of Gastroenterology2004，10，22： | 2 |
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