期刊文献+

全反式维甲酸诱导人肝癌细胞HepG2凋亡的初步研究 被引量:1

All-trans-retinoic Acid Induced Apoptosis of Human Hepatoma HepG2 Cells
原文传递
导出
摘要 [目的]研究全反式维甲酸(ATRA)体外诱导人肝癌细胞株HepG2的凋亡及其作用机制。[方法]ATRA处理HepG2细胞。MTT法分析细胞增殖反应;Hoechst染色法检测细胞凋亡情况;Western blot检测细胞中caspase-9、caspase-3和NF-κB蛋白表达情况。[结果]A-TRA可抑制HepG2细胞增殖并诱导细胞凋亡,可上调细胞中caspase-9、caspase-3表达水平(P<0.05)。[结论]ATRA可抑制HepG2细胞增殖并诱导细胞凋亡,其作用机制可能与cas-pase-9、caspase-3表达上调有关。 [Purpose] To investigate all-trans-retinoic acid (ATRA) induced apoptosis of human hepatoma HepG2 cells in vitro and its mechanism.[Methods] HepG2 cells line pretreated with ATRA.The proliferation of HepG2 was analyzed by MTT assay.The cell apoptosis was measured by Hoechst dye.The expressions of caspase-9,caspase-3 and NF-κB protein were detected by Western blot.[Results] ATRA could inhibit proliferation and induce apoptosis of HepG2 cell,Moreover,it could up-regulated caspase-9,caspase-3 expression level.[Conclusion] ATRA could inhibit proliferation and induce apoptosis of HepG2 cells and this effect maybe associated with upregulation of caspase-9 and caspase-3 expression.
出处 《肿瘤学杂志》 CAS 2010年第6期456-459,共4页 Journal of Chinese Oncology
基金 安徽省自然科学基金资助项目(050430705)
关键词 全反式维甲酸 HepG2细胞 凋亡 CASPASE-9 caspase-3 all-trans-retinoic acid HepG2 apoptosis caspase-9 caspase-3
  • 相关文献

参考文献4

二级参考文献89

  • 1王振义 孙关林 等.全反式维甲酸治疗急性早幼粒细胞白血病90例的临床研究[J].中华血液学杂志,1990,11(9):480-480.
  • 2[1]Chandrasekharan NV,Dai H,Roos KL,Evanson NK,Tomsik J,Elton TS,Simmons DL.COX-3,a cyclooxygenase-1 variant inhibited by acetaminophen and other analgesic/antipyretic drugs:cloning,structure,and expression.Proc Natl Acad Sci USA 2002; 99:13926-13931
  • 3[2]Zhang F,Warskulat U,Wettstein M,Schreiber R,Henninger HP,Decker K,Haussinger D.Hyperosmolarity stimulates prostaglandin synthesis and cyclooxygenase-2 expression in activated rat liver macrophages.Biochem J 1995; 312(Pt 1):135-143
  • 4[3]Feng L,Xia Y,Yoshimura T,Wilson CB.Modulation of neutrophil influx in glomerulonephritis in the rat with anti-macrophage inflammatory protein-2 (MIP-2) antibody.J Clin Invest 1995; 95:1009-1017
  • 5[4]Hussain T,Gupta S,Mukhtar H.Cyclooxygenase-2 and prostate carcinogenesis.Cancer Lett 2003; 191:125-135
  • 6[5]Peng JP,Su CY,Chang HC,Chai CY,Hung WC.Overexpression of cyclo-oxygenase-2 in squamous cell carcinoma of the hypopharynx.Hum Patho1 2002; 33:100-104
  • 7[6]Sheng H,Shao J,Morrow JD,Beauchamp RD,DuBois RN.Modulation of apoptosis and Bcl-2 expression by prostaglandin E2 in human colon cancer cells.Cancer Res 1998; 58:362-366
  • 8[7]Vogiagis D,Brown W,Glare EM,O'Brien PE.Rat colorectal tumours treated with a range of non-steroidal anti-inflammatory drugs show altered cyclooxygenase-2 and cyclooxygenase-1 splice variant mRNA expression levels.Carcinogenesis 2001; 22:869-874
  • 9[8]Leng J,Han C,Demetris AJ,Michalopoulos GK,Wu T.Cyclooxygenase-2 promotes hepatocellular carcinoma cell growth through Akt activation:evidence for Akt inhibition in celecoxib-induced apoptosis.Hepatology 2003; 38:756-768
  • 10[9]Kinoshita T,Takahashi Y,Sakashita T,Inoue H,Tanabe T,Yoshimoto T.Growth stimulation and induction of epidermal growth factor receptor by overexpression of cyclooxygenases 1 and 2 in human colon carcinoma cells.Biochem Biophys Acta 1999; 1438:120-130

共引文献44

同被引文献11

引证文献1

二级引证文献4

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部