中国药理学通报2011，Vol.27Issue(11)：1514-1517,4.DOI:10.3969/j.issn.1001-1978.2011.11.010
乙肝病毒x蛋白结合蛋白抑制阿霉素诱导HepG2细胞凋亡的机制研究
Overexpression of hepatitis B virus x-interacting protein in HepG2 cells inhibits apoptosis induced by doxorubicin hydrochloride
摘要
Abstract
Aim To investigate the effects of the expression of HBXIP protein in hepatoma cancer cell on the apoptosis induced by DOX. Methods MTT assay was used to assess the cell viability, DAPI and Annex-in V/PI were used to observe the apoptotic cells. Western blot was employed to detect the expression of protein. Results HepG2 cells with stable overexpres-sion HBXIP gene ( HepG2-hbxip ) exhibited higher resistance to DOX than did the vector-only transfected cell line ( pCMV-tag2B ). Annexin V/PI and apoptotic bodies formation assay after DOX treatment revealedapoptotic occuring in control cell pCMV-tag2B, whereas HepG2-hbxip cell showed a marked inhibition of apoptosis. Western blot results indicated that HBXIP inhibited DOX induced the activation of caspase cascade and its downstream effectors, Poly ( ADP-ribose ) poly-merase ( PARP). Conclusion HBXIP inhibits DOX-induced HepG2 cell apoptosis and cell death, which suggests that HBXIP may be considered as a target gene for treatment of hepatoma.关键词
肝细胞癌/乙肝病毒x蛋白结合蛋白/阿霉素/细胞凋亡/胱天蛋白酶/Bcl-2Key words
hepatocellular carcinoma/ HBXIP/ DOX/ cell apoptosis/ caspase/ bcl-2分类
医药卫生引用本文复制引用
王凤泽,费洪荣,张显忠,高丽君..乙肝病毒x蛋白结合蛋白抑制阿霉素诱导HepG2细胞凋亡的机制研究[J].中国药理学通报,2011,27(11):1514-1517,4.基金项目
国家自然科学基金资助项目(No 30800422) （No 30800422）
泰山医学院博士基金资助项目 （）
