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罗汉果山萘酚抑制hepg2细胞增殖潜在分子机制的探析

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中国细胞生物学学报 2024年第6期46卷 1121-1132页

作者：柯飞燕张定国罗贵钊伍志伟伊犁师范大学生物科学与技术学院伊宁835000 桂林医学院基础医学院桂林541199

利用网络药理学–分子对接结合细胞实验探讨罗汉果抑制肝细胞癌(hepatocellular carcinoma,HCC)的潜在分子机制。应用中药系统药理学数据库(TCMSP)筛选罗汉果活性成分与靶点,Genecards数据库检索肝细胞癌相关靶点,二者靶点经Venny平台... 详细信息

利用网络药理学–分子对接结合细胞实验探讨罗汉果抑制肝细胞癌(hepatocellular carcinoma,HCC)的潜在分子机制。应用中药系统药理学数据库(TCMSP)筛选罗汉果活性成分与靶点,Genecards数据库检索肝细胞癌相关靶点,二者靶点经Venny平台取交集,得到罗汉果治疗肝细胞癌的潜在靶点。以潜在作用靶点为基础,利用DAVID数据库进行基因功能和通路(GO/KEGG)富集分析后,采用Cytoscape软件构建罗汉果治疗肝细胞癌的“药物–成分–疾病–靶点”和“药物成分–靶点–通路–疾病”网络图,经生物分子功能注释系统数据库和Cytoscape软件获得核心作用靶点。选择药物活性成分(山萘酚)和关键靶点,运用AutoDock Vina软件进行分子对接。以山萘酚为实验药物、hepg2为研究对象,采用CCK-8法筛选其抑制hepg2细胞增殖的有效浓度,流式细胞术检测细胞凋亡率,Western blot检测潜在作用靶点的蛋白表达水平。筛选出罗汉果有效成分11个、作用靶点77个,肝细胞癌的疾病靶点7773个,二者共有靶点62个;GO与KEGG功能富集分析得到275个生物功能单位和87条信号通路;筛选出罗汉果抑制肝癌细胞增殖的潜在核心靶点p65、JNK1、Caspase-3、AKT1等10个;20μg/mL以上的罗汉果山萘酚能显著降低hepg2细胞的增殖活性和提高细胞凋亡率,显著上调p65、Caspase-3表达水平和下调JNK1、AKT1表达水平。罗汉果山萘酚具有抑制肝癌细胞增殖和促进其凋亡的活性,然而罗汉果具有多成分、多靶点、多通路的功效和作用特点,提示罗汉果治疗肝细胞癌的机制较为复杂。

关键词：网络药理学细胞增殖山萘酚肝癌 hepg2

EGFR siRNA序列的筛选及其对hepg2细胞活性的影响

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分子诊断与治疗杂志 2024年第5期16卷 935-939,944页

作者：许楠杨旭东薛丽宁启兰王慧莲耿燕西安交通大学第二附属医院医学检验科陕西西安710004 西安交通大学医学部遗传与分子生物学系陕西西安710061

目的构建EGFR shRNA重组真核表达载体,并筛选抑制效果最好的EGFR shRNA序列。方法应用在线工具设计人EGFR siRNA序列,采用限制性内切酶BamHI和HindIII切割真核表达质粒pcDNA3.1(+),构建三种人EGFR的siRNA干扰序列载体(psilencer 4.1-CMV... 详细信息

目的构建EGFR shRNA重组真核表达载体,并筛选抑制效果最好的EGFR shRNA序列。方法应用在线工具设计人EGFR siRNA序列,采用限制性内切酶BamHI和HindIII切割真核表达质粒pcDNA3.1(+),构建三种人EGFR的siRNA干扰序列载体(psilencer 4.1-CMV neo-EGFR siRNA)。将重组质粒载体转化大肠杆菌DH5α感受态并筛选阳性克隆,通过DNA测序鉴定重组质粒。应用脂质体lipo2000将三种人EGFR siRNA干扰序列载体转染到hepg2细胞,通过荧光显微镜观察转染效率,实时定量PCR检测EGFR mRNA表达水平,MTT法检测细胞活性。结果Psilencer 4.1-CMV neo-EGFR siRNA重组质粒被成功克隆。EGFR shRNA-1、EGFR shRNA-2和EGFR shRNA-3敲低EGFR mRNA的效率分别是80%、60%和70%以上。shRNA-2和shRNA-3使细胞活性分别下降50%(P0.05)。结论重组psilencer 4.1-CMV neo-EGFR siRNA质粒可下调肝癌细胞株EGFR表达水平和细胞活性。EGFR shRNA-3较EGFR shRNA-1和shRNA-2对hepg2细胞的抑制作用更显著。

关键词：基因治疗肝癌 hepg2 EGFR 小干扰RNA

基于转录组测序技术分析补骨脂素对hepg2细胞的作用机制

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临床输血与检验 2024年第1期26卷 35-41页

作者：汪思云李艺博谭春霞卢涛北京中医药大学生命科学学院北京102488

目的利用转录组测序(RNA-sequencing,RNA-seq)技术分析补骨脂素对肝癌hepg2细胞的作用机制。方法利用CCK-8法检测不同浓度的补骨脂素(0、62.5、125、250、500μM)作用hepg2细胞12 h和24 h后存活率的变化;流式细胞术检测250μM补骨脂素对... 详细信息

目的利用转录组测序(RNA-sequencing,RNA-seq)技术分析补骨脂素对肝癌hepg2细胞的作用机制。方法利用CCK-8法检测不同浓度的补骨脂素(0、62.5、125、250、500μM)作用hepg2细胞12 h和24 h后存活率的变化;流式细胞术检测250μM补骨脂素对hepg2细胞处理24 h后细胞周期的变化;RNA-seq测序获得对照组和补骨脂素组差异表达基因并进行GO富集分析和KEGG通路分析;实时荧光定量PCR技术验证差异基因表达水平。结果与对照组相比,补骨脂素作用hepg2细胞后,其存活率明显下降(P286个差异显著基因,其中包括130个上调基因和156个下调基因;GO功能富集和KEGG信号通路主要集中在细胞周期相关生物学过程及信号通路;qPCR结果显示hepg2细胞经补骨脂素处理后p 53和GADD 45B基因上调(P2、RRM2和CCND 1基因下调(Phepg2细胞产生毒性,阻滞细胞周期进程,其作用机制可能与调控细胞周期相关基因(p 53,CDK2,GADD45B,CCND1,RRM2)的表达有关。

关键词：补骨脂素 hepg2 RNA测序细胞周期

二氢辣椒碱对肝细胞癌细胞hepg2内apoM表达的影响

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哈尔滨医药 2024年第4期44卷 5-7页

作者：宋长悦樊小刚刘洪媛王全李成镇黑龙江省医院放射科沈阳国际旅行卫生保健中心上海市儿童医院超声科

目的观察二氢辣椒碱对肝细胞癌细胞hepg2的抑制作用，并探讨其分子机制。方法分为空白组和二氢辣椒碱（100μmol/1、150μmol/L、200μmol/L、250μmol/L）组，应用细胞计数法（CCK-8）检测在不同时间点（24h、48h、72h）、不同浓度... 详细信息

目的观察二氢辣椒碱对肝细胞癌细胞hepg2的抑制作用，并探讨其分子机制。方法分为空白组和二氢辣椒碱（100μmol/1、150μmol/L、200μmol/L、250μmol/L）组，应用细胞计数法（CCK-8）检测在不同时间点（24h、48h、72h）、不同浓度二氢辣椒碱（100μmol/L、150μmol/L、200μmol/L、250μmol/L）作用下肝细胞癌细胞hepg2的活性及数量变化；应用荧光定量PCR法（RT-PCR）检测在不同浓度二氢辣椒碱（150μmol/L、200μmol/L、250μmol/L）作用于肝细胞癌细胞hepg2 24h后，细胞内apoM m RCR的表达水平；应用免疫吸附测定法（ELISA）观察在不同浓度二氢辣椒碱（150μmol/L、200μmol/L、250μmol/L）作用于肝细胞癌细胞hepg2 24h后，细胞上清内的apoM水平。结果与空白组相比，二氢辣椒碱的浓度在100μmol/L时，其在各时间点（24、48、72h）的差异都无统计学意义，其余浓度二氢辣椒碱（150μmol/L、200μmol/L、250μmol/L）在各时间点（24、48、72h）差异均有统计学意义，提示肝细胞癌细胞hepg2对于二氢辣椒碱具有一定的时间及浓度依赖效应；与空白组相比，在浓度为150μmol/L、200μmol/L、250μmol/L的二氢辣椒碱作用下，肝细胞癌细胞hepg2内的apoM mRNA表达水平明显下调，且肝细胞癌细胞hepg2上清内的apoM水平也有下降（P_均hepg2具有抑制作用，且其抑制作用可能与抑制肝细胞癌细胞hepg2内的apoM表达有关。

关键词：二氢辣椒碱肝细胞癌 hepg2 载脂蛋白细胞凋亡

巨噬细胞迁移抑制因子通过调节AMPK信号通路改善hepg2细胞的胰岛素抵抗

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巨噬细胞迁移抑制因子通过调节AMPK信号通路改善HepG2细胞的胰岛...

Hepatoma cell line hepg2.2.15 demonstrates distinct biological features compared with parental hepg2

第七届全国康复与临床药学学术交流会议

作者：郝杨敏刘华杜国利新疆医科大学第一附属医院内分泌科

探索巨噬细胞迁移抑制因子(MIF)改善肝细胞胰岛素抵抗(insulin resistance,IR)的作用和机制。方法:通过高浓度胰岛素诱导体外胰岛素抵抗模型建立的方法,设置不同胰岛素浓度(0,10-9,10-8,10-7,10-6,10-5mol/L)处理人肝癌hepg2细胞建立IR... 详细信息

探索巨噬细胞迁移抑制因子(MIF)改善肝细胞胰岛素抵抗(insulin resistance,IR)的作用和机制。方法:通过高浓度胰岛素诱导体外胰岛素抵抗模型建立的方法,设置不同胰岛素浓度(0,10-9,10-8,10-7,10-6,10-5mol/L)处理人肝癌hepg2细胞建立IR模型,采用葡萄糖氧化酶法检测细胞的葡萄糖消耗量以及cck-8法测吸光值计算细胞活性来确定胰岛素浓度。设置不同的人重组巨噬细胞迁移抑制因子(rMIF)浓度梯度(0,25,50,100,200ng/ml)处理胰岛素抵抗模型24h,使用Westing blot蛋白质印迹检测rMIF不同浓度对于胰岛素抵抗模型,p-AKT和p-PI3K蛋白的表达。使用MIF敲低慢病毒转染(MIF shRNA)胰岛素抵抗模型细胞。最后采用用葡萄糖氧化酶法检测四组细胞的葡萄糖消耗量,RT-PCR技术检测细胞中InsR,PI3K,AKT,葡萄糖转运蛋白2(GLUT2),磷酸烯醇丙酮酸羧(PEPCK),葡萄糖-6-磷酸酶(G6Pase)的m RNA表达,Western blot技术检测细胞中IRS-1、p-PI3K、p-Akt的表达。结果:MIF显著增加Hep G2细胞的胰岛素抵抗模型的葡萄糖消耗,IR+rMIF组增加IRS-1蛋白表达水平,还增加了IRS-1,PI3K,GLUT2的m RNA相对表达量,降低了PEPCK、G6Pase的m RNA相对表达量。结论:MIF可改善hepg2细胞的胰岛素抵抗,其可能通过调控IRS-1/PI3K/Akt信号通路调节蛋白活性,促进糖原合成,降低血糖,改善胰岛素抵抗。

关键词：胰岛素抵抗 MIF hepg2 PEPCK 巨噬细胞迁移抑制因子信号通路

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World Journal of Gastroenterology 2011年第9期17卷 1152-1159页

作者： Ran Zhao Tian-Zhen Wang Dan Kong Lei Zhang Hong-Xue Meng Yang Jiang Yi-Qi Wu Zu-Xi Yu Xiao-Ming Jin Department of Pathology Harbin Medical University Harbin 150081 HeilongjiangProvince China Cancer Research Institute of Kanazawa UniversityKakuma-machi Kanazawa 920-1192 Japan National Heart Lung and Blood Institute NationalInstitutes of Health 9000 Rockville Pike Bethesda MD 20892United States

AIM:To investigate the biological features of hepatitis B virus(HBV)-transfected hepg2.2.15 cells. METHODS:The cell ultrastructure,cell cycle and apoptosis,and the abilities of proliferation and invasion of HBV-transfected hepg2.2.15 and the parent hepg2 cells were examined by electron microscopy,flow cytometry, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and trans-well *** of the two cell lines was compared via subcutaneous injection and orthotopic injection or implantation in nude mice,and the pathological analysis of tumor formation was *** cytoskeletal proteins were detected by Western blotting. RESULTS:Compared with hepg2 cells,hepg2.2.15 cells showed organelle degeneration and filopodia disappearance under electron ***2.2.15 cells proliferated and migrated slowly in vitro,and hardly formed tumor and lung metastasis in nude *** cytometry showed that the majority of hepg2.2.15 cells were arrested in G1 phase,and apoptosis was minor in both cell ***,the levels of cytoskeletal proteins F-actin and Ezrin were decreased in hepg2.2.15 cells. CONCLUSION:hepg2.2.15 cells demonstrated a lower proliferation and invasion ability than the hepg2 cells due to HBV transfection.

关键词： hepg2.2.15 hepg2 Hepatitis B virus Biological feature Tumor

Syringaresinol-4-O-β-D-glucoside alters lipid and glucose metabolism in hepg2 cells and C2C12 myotubes

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Acta Pharmaceutica Sinica B 2017年第4期7卷 453-460页

作者： Shuai Wang Chongming Wu Xin Li Yue Zhou Quanyang Zhang Fuchao Ma Jianhe Wei Xiaopo Zhang Peng Guo Institute of Medicinal Plant Development Chinese Academy of Medical Sciences & Peking Union Medical College Research Centre on Life Sciences and Environment Sciences Harbin University of Commerce School of Pharmaceutical Science Hainan Medical University

Syringaresinol-4-O-β-D-glucoside(SSG), a furofuran-type lignan, was found to modulate lipid and glucose metabolism through an activity screen of lipid accumulation and glucose consumption, and was therefore considered as a promising candidate for the prevention and treatment of metabolic disorder,especially in lipid and glucose metabolic homeostasis. In this study, the effects of SSG on lipogenesis and glucose consumption in Hep G2 cells and C2C12 myotubes were further investigated. Treatment with SSG significantly inhibited lipid accumulation by oil red O staining and reduced the intracellular contents of total lipid, cholesterol and triglyceride in Hep G2 cells. No effect was observed on cell viability in the MTT assay at concentrations of 0.1–10 μmol/L. SSG also increased glucose consumption by Hep G2 cells and glucose uptake by C2C12 myotubes. Furthermore, real-time quantitative PCR revealed that the beneficial effects were associated with the down-regulation of sterol regulatory element-binding proteins-1c,-2(SREBP-1c,-2), fatty acid synthase(FAS), acetyl CoA carboxylase(ACC) and hydroxyl methylglutaryl CoA reductase(HMGR), and up-regulation of peroxisome proliferator-activated receptors alpha and gamma(PPARα and PPARγ). SSG also significantly elevated transcription activity of PPARγtested by luciferase assay. These results suggest that SSG is an effective regulator of lipogenesis and glucose consumption and might be a candidate for further research in the prevention and treatment of lipid and glucose metabolic diseases.

关键词： Syringaresinol-4-O-β-d -glucoside Lipid accumulation Glucose consumption Insulin resistance hepg2 C2C12 Oil red O

Fermented Barley Extracts with Lactobacillus plantarum dy-1 Rich in Vanillic Acid Modulate Glucose Consumption in Human hepg2 Cells

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Biomedical and Environmental Sciences 2018年第9期31卷 667-676页

作者： ZHANG Jia Yan XIAO Xiang DONG Ying ZHOU Xing Hua School of Food and Biological Engineering Jiangsu University

Objective To investigate the effect of fermented barley extracts with Lactobacillus plantarum dy-1（LFBE） for modulating glucose consumption in hepg2 cells via miR-212 regulation. Methods Hepatocellular carcinoma（hepg2） cells were treated with palmitate. After 12 h, palmitate-induced hepg2 cells were treated with LFBE and its main components. Changes in glucose consumption, proinflammatory cytokine secretion, and miRNA-212 expression in hepg2 cells was observed. Results Treatment with LFBE rich in vanillic acid（VA） increased glucose consumption and reduced proinflammatory cytokine secretion in hepg2 cells. LFBE and VA normalized the upregulation of miR-212, which led to the upregulation of dual-specificity phosphatase-9（DUSP9）, a direct target of miR-212, at both protein and mR NA levels. Downregulation of miR-212 markedly increased glucose consumption and reduced proinflammatory cytokine secretion by enhancing DUSP9 expression. Conclusion The results showed the benefit of LFBE and miR-212 downregulation in modulating glucose consumption and reducing proinflammatory cytokine secretion by targeting DUSP9. VA in LFBE was a strong regulator of palmitate-induced abnormal glucose consumption in hepg2 cells and can be a primary mediator.

关键词： Fermented barley extract Vanillic acid Glucose consumption hepg2 Dual-specificity phosphatase-9

Pro-apoptotic effects of tectorigenin on human hepatocellular carcinoma hepg2 cells

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World Journal of Gastroenterology 2012年第15期18卷 1753-1764页

作者： Chun-Ping Jiang Hui Ding Da-Hua Shi Yu-Rong Wang Er-Guang Li Jun-Hua Wu The First Clinical Medical College NanjingUniversity of Chinese Medicine Nanjing 210046 Jiangsu Province China Department of Hepatobiliary Surgery The Affiliated Drum Tower Hospital Medical School Nanjing University Nanjing 210008 Jiangsu Province China Jiangsu Key Laboratory of Molecular Medicine State Key Laboratory of Pharmaceutical Biotechnology Medical School Nanjing University Nanjing 210093 Jiangsu Province China

AIM:To investigate the effects of tectorigenin on human hepatocellular carcinoma(HCC)hepg2 ***:Tectorigenin,one of the main components of rhizome of Iris tectorum,was prepared by simple methods,such as extraction,filtration,concentration,precipitation and ***2 cells were incubated with tectorigenin at different concentrations,and their viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide *** was detected by morphological observation of nuclear change,agarose gel electrophoresis of DNA ladder,and flow cytometry with Hoechst 33342,Annexin V-EGFP and propidium iodide *** of reactive oxygen species was quantified using *** Ca2+was monitored by Fura *** membrane potential was monitored using Rhodamine *** of cytochrome c from mitochondria to cytosol was detected by Western *** of caspase-3,-8 and-9 were investigated by Caspase Activity Assay ***:The viability of hepg2 cells treated by tectorigenin decreased in a concentration-and timedependent *** concentration that reduced the number of viable hepg2 cells by 50%(IC50)after 12,24 and 48 h of incubation was 35.72 mg/L,21.19 mg/L and 11.06 mg/L,***,treatment with tectorigenin at 20 mg/L resulted in a very slight cytotoxicity to L02 cells after incubation for 12,24 or 48 *** at a concentration of 20 mg/L greatly inhibited the viability of hepg2 cells and induced the condensation of chromatin and fragmentation of *** induced apoptosis of hepg2 cells in a time-and dose-dependent *** with the viability rate,induction of apoptosis was the main mechanism of the anti-proliferation effect of tectorigenin in hepg2 ***,tectorigenininduced apoptosis of hepg2 cells was associated with the generation of reactive oxygen species,increased intracellular[Ca2+]i,loss of mitochondrial membrane potential,transloca

关键词： Tectorigenin Iris tectorum maxim Apop-tosis Hepatocellular carcinoma hepg2 Mitochondria Liver cancer