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作 者:王标 陈艳 WANG Biao;CHEN Yan(Key Laboratory of Ministry of Education for Gastroin testinal Cane er,Key Laboratory of Fujian Province for Tumor Microbiology,School of Basic Medical Science,Fujian Medical University,Fuzhou 350122,China)
机构地区:[1]福建医科大学基础医学院,消化道恶性肿瘤教育部重点实验室,福建省肿瘤微生物学重点实验室,福州350122
出 处:《福建医科大学学报》2021年第2期99-103,共5页Journal of Fujian Medical University
基 金:国家自然科学基金青年项目(81702014);福建省自然科学基金面上项目(2018J01840);福建省卫生计生中青年骨干人才培养项目(2018-ZQN-58)。
摘 要:目的探讨乙型肝炎病毒(HBV)对晚期糖基化终产物受体(AGE-Rs)表达及AGEs诱导下肝癌细胞增殖的影响。方法利用HepG2.2.15细胞或肝癌细胞HepG2瞬时转染1.2倍HBV基因组,采用实时荧光定量PCR技术和蛋白质免疫印迹法(Western-blot),从mRNA水平和蛋白水平检测HBV对AGE-Rs表达的影响。使用AGEs(100μg/mL)处理细胞,采用CCK-8法比较HepG2和HepG2.2.15细胞在AGEs诱导下的增殖情况。结果在HepG2.2.15细胞或瞬时转染HBV的HepG2细胞中,AGE-R1和AGE-R3的mRNA和蛋白表达水平降低(P<0.05),而AGE-R2表达水平无变化。细胞增殖实验表明,在AGEs诱导下,HepG2.2.15细胞的增殖能力强于HepG2细胞(P<0.05)。结论HBV可以抑制肝癌细胞AGE-R1和AGE-R3的表达,并促进AGEs诱导下肝癌细胞的增殖。Objective To explore the effect of hepatitis B virus(HBV)on the expression of advanced glycation end products receptors(AGE-Rs)and the proliferation of hepatoma cells induced by AGEs.Methods With the use of HepG2.2.15 cells or hepatoma HepG2 cells transient transfected by 1.2×length of HBV genome,the influence of HBV on AGE-Rs expression at mRNA and protein levels was detected by Real-time PCR and Western-blot.The hepatoma cells were treated with 100μg/mL AGEs and the proliferation of HepG2 and HepG2.2.15 cells were compared by CCK-8 assay.Results In HepG2.2.15 cells or HepG2 cells transient transfected with HBV,the expression of AGE-R1 and AGE-R3 at mRNA and protein levels,but not of AGE-R2,were decreased(P<0.05).CCK-8 assay displayed that the proliferation rate of HepG2.2.15 cells was higher than that of HepG2 cells under the treatment of AGEs(P<0.05).Conclusion HBV can inhibit the expression of AGE-R1 and AGE-R3 in liver cells and promote the proliferation of hepatoma cells induced by AGEs.
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