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EZH2 inhibitors promote β-like cell regeneration in young and adult type 1 diabetes donors

Signal Transduction and Targeted Therapy 2024年第2期9卷 679-692页

作者： Keith Al-Hasani Safiya Naina Marikar Harikrishnan Kaipananickal Scott Maxwell jun okabe Ishant Khurana Thomas Karagiannis Julia J.Liang Lina Mariana Thomas Loudovaris Thomas Kay Assam El-Osta Epigenetics in Human Health and Disease Program Baker Heart and Diabetes Institute75 Commercial RoadMelbourne 3004 VICAustralia Department of Diabetes Central Clinical SchoolMonash UniversityMelbourne 3004 VICAustralia Epigenetics in Human Health and Disease Laboratory Central Clinical SchoolMonash UniversityMelbourne 3004 VICAustralia School of Science STEM CollegeRMIT UniversityMelbourne 3001 VICAustralia Immunology and Diabetes Unit St Vincent’s Institute of Medical ResearchFitzroy 3065 VICAustralia Department of Medicine and Therapeutics The Chinese University of Hong KongSha TinHong Kong SAR Hong Kong Institute of Diabetes and Obesity Prince of Wales HospitalThe Chinese University of Hong Kong3/F Lui Che Woo Clinical Sciences Building30-32-Ngan Shing StreetSha TinHong Kong SAR Li Ka Shing Institute of Health Sciences The Chinese University of Hong KongSha TinHong Kong SAR Biomedical Laboratory Science Department of TechnologyFaculty of HealthUniversity College CopenhagenCopenhagenDenmark

β-cells are a type of endocrine cell found in pancreatic islets that synthesize,store and release insulin.In type 1 diabetes(T1D),T-cells of the immune system selectively destroy the insulin-producingβ-cells.Destruction of these cells leads to a lifelong dependence on exogenous insulin administration for survival.Consequently,there is an urgent need to identify novel therapies that stimulateβ-cell growth and induceβ-cell function.We and others have shown that pancreatic ductal progenitor cells are a promising source for regeneratingβ-cells for T1D owing to their inherent differentiation capacity.Default transcriptional suppression is refractory to exocrine reaction and tightly controls the regenerative potential by the EZH2 methyltransferase.In the present study,we show that transient stimulation of exocrine cells,derived from juvenile and adult T1D donors to the FDAapproved EZH2 inhibitors GSK126 and Tazemetostat(Taz)influence a phenotypic shift towards aβ-like cell identity.The transition from repressed to permissive chromatin states are dependent on bivalent H3K27me3 and H3K4me3 chromatin modification.Targeting EZH2 is fundamental toβ-cell regenerative potential.Reprogrammed pancreatic ductal cells exhibit insulin production and secretion in response to a physiological glucose challenge ex vivo.These pre-clinical studies underscore the potential of small molecule inhibitors as novel modulators of ductal progenitor differentiation and a promising new approach for the restoration ofβ-like cell function.

关键词： EZH2 struction inhibitors

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Inhibition of pancreatic EZH2 restores progenitor insulin in T1D donor

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Signal Transduction and Targeted Therapy 2022年第8期7卷 3045-3053页

作者： Keith Al-Hasani Ishant Khurana Lina Mariana Thomas Loudovaris Scott Maxwell K.N.Harikrishnan jun okabe Mark ECooper Assam El-Osta Department of Diabetes Central Clinical SchoolMonash UniversityMelbourneVictoria 3004Australia Epigenetics in Human Health and Disease Laboratory Central Clinical SchoolMonash UniversityMelbourneVictoria 3004Australia Immunology and Diabetes Unit St Vincent’s Institute of Medical ResearchFitzroyVictoriaAustralia Department of Clinical Pathology The University of MelbourneParkvilleVictoriaAustralia Department of Medicine and Therapeutics The Chinese University of Hong KongSha TinHong Kong SAR Hong Kong Institute of Diabetes and Obesity Prince of Wales HospitalThe Chinese University of Hong Kong3/F Lui Che Woo Clinical Sciences Building30-32 Ngan Shing StreetSha TinHong Kong SAR Li Ka Shing Institute of Health Sciences The Chinese University of Hong KongSha TinHong Kong SAR Faculty of Health Department of TechnologyBiomedical Laboratory ScienceUniversity College CopenhagenCopenhagenDenmark

Type 1 diabetes(T1D)is an autoimmune disease that selectively destroys insulin-producingβ-cells in the pancreas.An unmet need in diabetes management,current therapy is focussed on transplantation.While the reprogramming of progenitor cells into functional insulin-producingβ-cells has also been proposed this remains controversial and poorly understood.The challenge is determining why default transcriptional suppression is refractory to exocrine reactivation.After the death of a 13-year-old girl with established insulin-dependent T1D,pancreatic cells were harvested in an effort to restore and understand exocrine competence.The pancreas showed classic silencing ofβ-cell progenitor genes with barely detectable insulin(Ins)transcript.GSK126,a highly selective inhibitor of EZH2 methyltransferase activity influenced H3K27me3 chromatin content and transcriptional control resulting in the expression of coreβ-cell markers and ductal progenitor genes.GSK126 also reinstated Ins gene expression despite absoluteβ-cell destruction.These studies show the refractory nature of chromatin characterises exocrine suppression influencingβ-cell plasticity.Additional regeneration studies are warranted to determine if the approach of this n-of-1 study generalises to a broader T1D population.

关键词： EZH2 progenitor donor

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SAHA attenuates Takotsubo-like myocardial injury by targeting an epigenetic Ac/Dc axis

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Signal Transduction and Targeted Therapy 2021年第5期6卷 1429-1432页

作者： Ishant Khurana Scott Maxwell Simon Royce Prabhu Mathiyalagan Tom Karagiannis Nadia Mazarakis Jitraporn Vongsvivut Harikrishnan K.N. jun okabe Keith Al-Hasani Chrishan Samuel Assam El-Osta Human Epigenetics Program Department of DiabetesCentral Clinical SchoolMonash UniversityMelbourneVICAustralia Cardiovascular Disease Program Monash Biomedicine Discovery Institute and Department of PharmacologyMonash UniversityClaytonVICAustralia Infrared Microspectroscopy Beamline ANSTO-Australian SynchrotronClaytonVICAustralia Department of Medicine and Therapeutics The Chinese University of Hong Kong(CUHK)Hong Kong SARHong Kong Institute of Diabetes and ObesityCUHKHong Kong SARPrince of Wales HospitalLi Ka Shing Institute of Health SciencesCUHKShatinHong KongChina University College Copenhagen Faculty of HealthDepartment of TechnologyBiomedical Laboratory ScienceCopenhagenDenmark

Dear Editor,Takotsubo syndrome(TS)is a stress-induced non-ischaemic cardiomyopathy that is more common in women,but is associated with higher morbidity and mortality in males.Also known as broken-heart syndrome,TS is characterised by transient left ventricular(LV)dysfunction independent of obstructive coronary artery disease.TS is a polygenic condition and nowhere is this more evident than the use of positive inotropes,such as isoprenaline(ISO)in pre-clinical models.1 There is no standard therapy for broken-heart syndrome because the mechanisms underlying the condition remain unknown.Furthermore,there is no consensus on predisposition for Takotsubo2 and our goal was to better understand the regulatory mechanism as a first step towards improved treatment plans.Suberanilohydroxamic acid or SAHA,a drug approved for cancer treatment by the US Food and Drug Administration has previously been shown to improve cardiopulmonary function.3 We tested the hypothesis that the cardioprotective benefit of SAHA in a pre-clinical model of Takotsubo is conferred by an epigenetic acetylation/deacetylation(Ac/Dc)axis.

关键词： SAHA Takotsubo protective

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Intraductal neoplasm of the intrahepatic bile duct: Clinicopathological study of 24 cases

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World Journal of Gastroenterology 2012年第28期18卷 3673-3680页

作者： Yoshiki Naito Hironori Kusano Osamu Nakashima Eiji Sadashima Satoshi Hattori Tomoki Taira Akihiko Kawahara Yoshinobu okabe Kazuhide Shimamatsu jun Taguchi Seiya Momosaki Koji Irie Rin Yamaguchi Hiroshi Yokomizo Michiko Nagamine Seiji Fukuda Shinichi Sugiyama Naoyo Nishida Koichi Higaki Munehiro Yoshitomi Masafumi Yasunaga Koji Okuda Hisafumi Kinoshita Masayoshi Kage Masamichi Nakayama Makiko Yasumoto jun Akiba Hirohisa Yano Departments of Pathology Kurume University School of Medicine Kurume 830-0011 Japan Biostatistics Center Kurume University Kurume 830-0011 Japan Department of Diagnostic Pathology Kurume University Hospital Kurume 830-0011 Japan Division of Gastroenterology Department of Medicine Kurume University School of Medicine Kurume 830-0011 Japan Department of Pathology Omuta City General Hospital Omuta 836-8567 Japan Department of Pathology Asakura Medical Association Hospital Fukuoka 838-0069 Japan Department of Pathology National Hospital Organization Kyushu Medical Center Fukuoka 810-8563 Japan Department of Pathology Shin-Koga Hospital Tenjinkai 120 Tenjincho Kurume 830-0033 Japan Department of Pathology Kurume University Medical Center 155-1 Kokubumachi Kurume 839-0863 Japan Department of Surgery Japanese Red Cross Kumamoto Hospital Kumamoto 861-8520 Japan Department of Pathology Japanese Red Cross Kumamoto Hospital Kumamoto 861-8520 Japan Division of Surgery Saiseikai Kumamoto Hospital Kumamoto 861-4193 Japan Department of Pathology St Mary's Hospital Kurume 830-8543 Japan Department of Surgery Kurume University School of Medicine Kurume 830-0011 Japan

AIM: To investigate the clinicopathological features of intraductal neoplasm of the intrahepatic bile duct (INihB). METHODS: Clinicopathological features of 24 cases of INihB, which were previously diagnosed as biliary papillomatosis or intraductal growth of intrahepatic biliary neoplasm, were reviewed. Mucin immunohistochemistry was performed for mucin (MUC)1, MUC2, MUC5AC and MUC6. Ki-67, P53 and β-catenin immunoreactivity were also examined. We categorized each tumor as adenoma (low grade), borderline (intermediate grade), and malignant (carcinoma in situ , high grade including tumors with microinvasion). RESULTS: Among 24 cases of INihB, we identified 24 tumors. Twenty of 24 tumors (83%) were composed of a papillary structure; the same feature observed in intraductal papillary neoplasm of the bile duct (IPNB). In contrast, the remaining four tumors (17%) showed both tubular and papillary structures. In three of the four tumors (75%), macroscopic mucin secretion was limited but microscopic intracellular mucin was evident. Histologically, 16 tumors (67%) were malignant, three (12%) were borderline, and five (21%) were adenoma. Microinvasion was found in four cases (17%). Immunohistochemical analysis revealed that MUC1 was not expressed in the borderline/adenoma group but was expressed only in malignant lesions (P = 0.0095). Ki-67 labeling index (LI) was significantly higher in the malignant group than in the borderline/adenoma group (22.2 ± 15.5 vs 7.5 ± 6.3, P < 0.01). In the 16 malignant cases, expression of MUC5AC showed borderline significant association with high Ki-67 LI (P = 0.0622). Nuclear expression of β-catenin was observed in two (8%) of the 24 tumors, and these two tumors also showed MUC1 expression. P53 was negative in all tumors. CONCLUSION: Some cases of INihB have a tubular structure, and are subcategorized as IPNB with tubular structure. MUC1 expression in INihB correlates positively with degree of malignancy.

关键词：胆管肿瘤临床病理管内免疫组织化学方法恶性肿瘤管状结构乳头状瘤肝

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基于网络药理学及动物实验探讨景芪愈溃胶囊提高胃溃疡黏膜愈合质量的作用及机制

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中国中药杂志 2022年第5期47卷 1350-1358页

作者：范珉珏段永强李能莲杨晓轶马骏巩子汉王道坤甘肃中医药大学基础医学院甘肃兰州730000 宁夏医科大学宁夏银川750004 敦煌医学与转化教育部重点实验室甘肃兰州730003 中国中医科学院中医基础理论研究所北京100700

该研究通过网络药理学预测景芪愈溃胶囊治疗胃溃疡的活性成分及作用机制并采用动物实验进一步验证部分关键靶点及信号通路,探讨景芪愈溃胶囊对胃溃疡的治疗效果及机制。首先通过BATMAN-TCM(Bioinformatics Analysis Tool for Molecular ... 详细信息

该研究通过网络药理学预测景芪愈溃胶囊治疗胃溃疡的活性成分及作用机制并采用动物实验进一步验证部分关键靶点及信号通路,探讨景芪愈溃胶囊对胃溃疡的治疗效果及机制。首先通过BATMAN-TCM(Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine)、TCMSP(Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform)下载得到景芪愈溃胶囊活性成分及作用靶点,通过GeneCards和OMIM(Online Mendelian Inheritance in Man)以“gastric ulcer”为关键词检索获取疾病靶点,将成分靶点和疾病靶点取交集,获得景芪愈溃胶囊治疗胃溃疡的潜在靶点。随后利用STRING在线数据库及Cytoscape 3.7.2软件构建靶点的PPI(protein-protein interaction)网络图并分析,利用Matescape数据库进行KEGG(Kyoto Encyclopedia of Genes and Genomes)信号通路富集分析并利用Omicshare在线分析平台进行富集通路可视化处理。最后采用改良okabe法构建胃溃疡大鼠模型,分别使用高、中、低剂量的景芪愈溃胶囊,安胃疡胶囊以及雷贝拉唑钠肠溶胶囊进行干预,肉眼观察溃疡情况,采用HE染色观察大鼠胃组织形态学变化,采用考马斯亮蓝法检测大鼠胃组织iNOS的含量,综合评价大鼠胃溃疡的溃疡愈合质量;采用RT-qPCR及Western blot检测大鼠胃组织中部分蛋白的基因及蛋白的表达水平,进一步验证部分关键靶点及信号通路。经数据库分析获得景芪愈溃胶囊活性成分206个,作用靶点535个,胃溃疡的作用靶点1 305个,药物和疾病交集靶点166个。PPI网络分析以及KEGG通路富集分析显示,多个关键靶蛋白IL6、TNF、MAPK1、MAPK3、MAPK14等,以及前20条关键信号通路中的NF-κB signaling pathway、IL-17 signaling pathway、leukocyte transendothelial migration与炎症关系密切;动物实验选取关键蛋白p38 MAPK以及经典的炎症信号通路NF-κB signaling pathway进行进一步动物实验验证,景芪愈溃胶囊高剂量组大鼠胃溃疡的恢复情况最接近空白组,胃组织iNOS含量显著降低,p38 MAPK基因和磷酸化、NF-κB p65基因和蛋白表达水平显著降低。提示景芪愈溃胶囊可抑制关键蛋白p38 MAPK的磷酸化和NF-κB信号通路中NF-κB p65的表达以发挥抗炎的作用,并可有效提高胃溃疡大鼠的溃疡愈合质量,验证了网络药理学的部分预测结果。

关键词：网络药理学景芪愈溃胶囊胃溃疡溃疡愈合质量炎症

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景芪愈溃胶囊对脾胃虚寒型胃溃疡大鼠的作用及其机制

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中国病理生理杂志 2021年第9期37卷 1596-1602页

作者：范珉珏段永强虎峻瑞罗强杨晓轶李能莲马骏巩子汉甘肃中医药大学基础医学院甘肃兰州730000 甘肃中医药大学敦煌医学与转化教育部重点实验室甘肃兰州730000 甘肃中医药大学中医方药挖掘与创新转化重点实验室甘肃兰州730000 中国中医科学院中医基础理论研究所北京100700

目的:研究景芪愈溃胶囊对脾胃虚寒型胃溃疡大鼠的影响并探讨其机制。方法:将70只SPF级Wistar大鼠按完全随机设计分为空白组和造模组,造模组采用大黄苦寒泻下法+饥饱失常喂养法+改良okabe法综合因素构建脾胃虚寒型胃溃疡大鼠模型,造模成... 详细信息

目的:研究景芪愈溃胶囊对脾胃虚寒型胃溃疡大鼠的影响并探讨其机制。方法:将70只SPF级Wistar大鼠按完全随机设计分为空白组和造模组,造模组采用大黄苦寒泻下法+饥饱失常喂养法+改良okabe法综合因素构建脾胃虚寒型胃溃疡大鼠模型,造模成功后按随机数字表法分为模型组,景芪愈溃胶囊高、中、低剂量组,中药阳性对照(安胃疡胶囊)组,以及西药阳性对照(雷贝拉唑钠肠溶胶囊)组。空白组和模型组给予2 mL/d蒸馏水灌胃,其余各药物干预组分别给予对应剂量的胶囊内容物混悬液2 mL/d灌胃,持续干预14 d。使用游标卡尺测量胃溃疡最大长径并计算溃疡指数(UI);采用HE染色观察大鼠胃组织形态学变化;采用ELISA法检测大鼠胃组织中白细胞介素1(IL-1)、IL-4、IL-6和IL-13的含量;采用RT-qPCR法检测大鼠胃组织中血管细胞黏附因子1(VCAM-1)和细胞间黏附分子1(ICAM-1)的mRNA表达水平,并采用Western blot法检测大鼠胃组织中上述指标的蛋白相对表达水平。结果:与空白组比较,模型组大鼠胃黏膜可见明显溃疡面,光镜下观察可见黏膜组织缺失和坏死,胃组织IL-1和IL-6含量明显升高,IL-4和IL-13含量明显降低,VCAM-1和ICAM-1的mRNA和蛋白表达水平显著升高(P<0.01);与模型组比较,景芪愈溃胶囊高剂量组大鼠的UI显著降低,光镜下观察胃溃疡的恢复情况最接近空白组,胃组织IL-1和IL-6含量显著降低,IL-4和IL-13含量显著升高,VCAM-1和ICAM-1的mRNA和蛋白表达水平显著降低(P<0.01)。结论:景芪愈溃胶囊可有效促进胃溃疡的愈合,其机制可能与抑制细胞黏附分子VCAM-1和ICAM-1表达进而减少促炎因子IL-1和IL-6含量,增加抗炎因子IL-4和IL-13含量,从而调节促炎因子与抗炎因子的平衡有关。

关键词：景芪愈溃胶囊胃溃疡炎症血管细胞黏附因子1 细胞间黏附分子1

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整体刚性面板加筋土挡墙振动台模型试验研究

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岩土力学 2019年第3期40卷 998-1004页

作者：徐鹏蒋关鲁邱俊杰高泽飞王智猛西南交通大学土木工程学院四川成都610031 西南交通大学高速铁路线路工程教育部重点试验室四川成都610031 中铁二院工程集团有限责任公司四川成都610031

加筋土挡墙在大量地震中显示了优越的抗震性能。地震荷载作用下,加筋土挡墙的设计中通常采用拟静力法将动荷载等效为静力荷载。为了对比加筋土挡墙拟静力设计值与实际动力响应值的差异,开展了整体刚性面板加筋土挡墙振动台模型试验。通... 详细信息

加筋土挡墙在大量地震中显示了优越的抗震性能。地震荷载作用下,加筋土挡墙的设计中通常采用拟静力法将动荷载等效为静力荷载。为了对比加筋土挡墙拟静力设计值与实际动力响应值的差异,开展了整体刚性面板加筋土挡墙振动台模型试验。通过位移、加速度、土压力、筋材拉力的测试,得到以下结论:加筋土挡墙内部的加速度分布不均匀并呈现面板、加筋体加速度大于填土加速度的趋势,同时测试的响应加速度值大于设计规范建议值;面板背面土压力作用点高于设计值,但合力仅为物部-冈部理论值的15%～20%;受加速度放大效应及动土压力作用点的影响,墙体的主要变形模式为转动变形;筋材拉力沿墙高非线性分布并且测试合力大于铁路规范建议值。

关键词：加筋土挡墙地震拟静力法振动台模型试验加速度

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甘肃地区番茄细菌性斑点病菌的鉴定与检测

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中国蔬菜 2013年第3X期 68-73页

作者：文朝慧王军平何苏琴甘肃出入境检验检疫局甘肃兰州730020 甘肃省农业科学院植物保护研究所甘肃兰州730070

从番茄病果上分离纯化的细菌菌株,经致病性测定、形态特征、培养特性观察及16S rDNA序列测定,鉴定为番茄细菌性斑点病菌Pseudomonas syringae pv.tomato(okabe)Young,Dye et Wilkie。利用特异性引物对已鉴定菌株及番茄发病组织进行PCR扩... 详细信息

从番茄病果上分离纯化的细菌菌株,经致病性测定、形态特征、培养特性观察及16S rDNA序列测定,鉴定为番茄细菌性斑点病菌Pseudomonas syringae pv.tomato(okabe)Young,Dye et Wilkie。利用特异性引物对已鉴定菌株及番茄发病组织进行PCR扩增,均扩增出530bp左右的特异性片段,印证了可利用特异性引物MM5F/MM5R对分离菌株或番茄发病组织进行PCR扩增以检测番茄细菌性斑点病菌。

关键词：番茄细菌性斑点病菌分离检测

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溃疡平对胃溃疡大鼠胃黏膜组织中VEGF和Flt-1 mRNA表达的影响

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北京中医药大学学报 2010年第7期33卷 476-479页

作者：朱立革曹军赵红晔周丽王滨齐齐哈尔医学院基础医学部黑龙江161006 黑龙江中医药大学研究生学院中国中医科学院中药研究所

目的观察溃疡平对胃溃疡大鼠胃黏膜组织血管内皮生长因子(VEGF)和血管内皮生长因子受体-1(Flt-1)mRNA表达的影响,探讨溃疡平促进大鼠胃溃疡愈合的机制。方法采用改良okabe法制备慢性乙酸胃溃疡模型,随机分为:正常对照组,模型对照组,溃... 详细信息

目的观察溃疡平对胃溃疡大鼠胃黏膜组织血管内皮生长因子(VEGF)和血管内皮生长因子受体-1(Flt-1)mRNA表达的影响,探讨溃疡平促进大鼠胃溃疡愈合的机制。方法采用改良okabe法制备慢性乙酸胃溃疡模型,随机分为:正常对照组,模型对照组,溃疡平高、中、低剂量(5.6、2.8、1.4g/kg)组,盐酸雷尼替丁(28.3mg/kg)组。给药治疗14d,采用实时荧光定量PCR法检测胃黏膜组织VEGF和Flt-1mRNA表达。结果与模型对照组相比,溃疡平中、高剂量组的VEGF2-ΔΔCT值明显增高,表明溃疡平中、高剂量组的VEGFmRNA表达上调,有统计学意义(P分别<0.05和<0.001);溃疡平高剂量组的Flt-12-ΔΔCT值明显增高,表明溃疡平高剂量组的Flt-1mRNA表达上调,有统计学意义(P<0.001)。结论溃疡平可促进胃溃疡大鼠胃黏膜组织VEGF和Flt-1mRNA表达,这可能是其促进溃疡愈合,提高溃疡愈合质量,减少溃疡复发的分子学机制之一。

关键词：溃疡平胃溃疡血管内皮生长因子血管内皮生长因子受体-1 实时荧光定量PCR 大鼠

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溃疡平对胃溃疡大鼠胃黏膜组织中EGF和EGFR mRNA表达的影响

引用

北京中医药大学学报 2008年第11期31卷 759-762页

作者：王滨赵红晔周丽王月飞曹军齐齐哈尔医学院生理教研室黑龙江161001 中国中医科学院中药研究所

目的观察溃疡平对胃溃疡大鼠胃黏膜组织表皮生长因子(EGF)和表皮生长因子受体(EG-FR)mRNA表达的影响,探讨溃疡平的促进胃溃疡愈合的机制。方法采用改良okabe法制备慢性乙酸胃溃疡模型;随机分为:实验对照组,模型组,溃疡平高、中、低剂量... 详细信息

目的观察溃疡平对胃溃疡大鼠胃黏膜组织表皮生长因子(EGF)和表皮生长因子受体(EG-FR)mRNA表达的影响,探讨溃疡平的促进胃溃疡愈合的机制。方法采用改良okabe法制备慢性乙酸胃溃疡模型;随机分为:实验对照组,模型组,溃疡平高、中、低剂量组,盐酸雷尼替丁组,共6组;给药治疗14 d,采用实时荧光定量PCR法检测胃黏膜组织EGF和EGFR mRNA表达。结果与模型组相比,溃疡平低、中、高剂量组的EGF 2-ΔΔCT值明显增高,表明溃疡平能使EGF mRNA表达上调,有统计学意义(P<0.01);溃疡平低、中、高剂量组的EGFR 2-ΔΔCT值明显增高,表明溃疡平能使EGFR mRNA表达上调,有统计学意义(P<0.001)。结论溃疡平可促进胃溃疡大鼠胃黏膜组织EGF和EGFR mRNA表达,这可能是其促进溃疡愈合,提高溃疡愈合质量,减少溃疡复发的分子学基础之一。

关键词：溃疡平胃溃疡表皮生长因子表皮生长因子受体实时荧光定量PCR 大鼠

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维普期刊数据库

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