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作 者:李小芳 张丹 宋大强 宋姗姗 刘明华 LI Xiao-fang;ZHANG Dan;SONG Da-qiang;SONG Shan-shan;LIU Ming-hua(Department of Antitumor Pharmacology,School of Pharmacy,Southwest Medical University,Sichuan Luzhou 646000,China;Department of Pharma-cy,The Affiliated Hospital of Southwest Medical University,Sichuan Luzhou 646000,China;Division of Antitumor Pharma-cology,State Key Laboratory of Drug Research,Shanghai Institute of Materia Medica,Chinese Academy of Sciences,Shanghai 201203,China)
机构地区:[1]西南医科大学药学院肿瘤药理实验室,四川泸州646000 [2]西南医科大学附属医院药学部,四川泸州646000 [3]中国科学院上海药物研究所新药研究国家重点实验室肿瘤药理研究室,上海201203
出 处:《中国医院药学杂志》2018年第18期1921-1925,共5页Chinese Journal of Hospital Pharmacy
基 金:四川省教育厅重点项目(编号:17ZA0429)
摘 要:目的:研究白术内酯Ⅰ(atractylenolideⅠ)对人胃癌细胞SGC-7901裸鼠移植瘤生长及凋亡相关蛋白Bax、cleaved caspase-3、p53、Bcl-2表达的影响。方法:建立SGC-7901裸鼠移植瘤模型,观察白术内酯Ⅰ对肿瘤生长的影响;TUNEL法检测移植瘤组织中的细胞凋亡;Western blotting检测瘤组织中Bax、Bcl-2、cleaved caspase-3及p53蛋白表达。结果:白术内酯Ⅰ不同程度抑制裸鼠SGC-7901移植瘤的生长,与对照组比较,给药后肿瘤体积(TV,tumor volume)、相对肿瘤体积(RTV,relative tumor volume)和相对肿瘤增殖率[T/C(%),TRTV/CRTV]明显下降;移植瘤组织中凋亡细胞明显增多;白术内酯Ⅰ上调移植瘤组织中Bax、cleaved caspase-3及p53的蛋白表达,下调Bcl-2的蛋白表达。结论:白术内酯Ⅰ能明显抑制人胃癌细胞SGC-7901裸鼠移植瘤的生长,分子机制主要包括增加Bax、cleaved caspase-3、p53蛋白表达,减少Bcl-2蛋白表达,最终导致肿瘤细胞凋亡。OBJECTIVE To investigate the effect of atractylenolideⅠ on the growth and expression of apoptosis related proteins involving Bax,cleaved caspase-3,p53 and Bcl-2 in human gastric cancer cell line SGC-7901 xenografts in nude mice.METHODS The model of nude mice with SGC-7901 cell was established significantly in the treatment group.The cell apoptosis of transplant tumor tissue increased as detected by the TUNEL assay.The expression of proteins including Bcl-2,Bax,cleaved caspase-3 and p53 were determined by Western blotting assay.RESULTS AtractylenolideⅠinhibited the growth of xenografts in nude mice.Compared with control group,TV(tumor volume),RTV(relative tumor volume)and T/C(%)(TRTV/CRTV)decreased after treatment with atractylenolide I.The apoptosis cells were elevated after treatment with atractylenolidesⅠ.Western blotting showed that several proteins including Bax,cleaved caspase-3 and p53 were up-regulated after treatment with atractylenolidesⅠ,however,the expression of Bcl-2 protein inversed in the transplant tumor tissues.CONCLUSION Atractylenolide I significantly inhibits the growth of SGC-7901 cell xenografts in nude mice,which may be caused by inducing tumor cell apoptosis by up-regulation of Bax,cleaved caspase-3,p53 expressions and down-regulation of Bcl-2 expression.
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