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雷公藤内酯醇对肝癌H22细胞增殖凋亡及COX-2表达的影响
引用本文:甘陈灵,邹玉莲,黄秀旺,许建华. 雷公藤内酯醇对肝癌H22细胞增殖凋亡及COX-2表达的影响[J]. 福建医科大学学报, 2017, 51(3): 146-149
作者姓名:甘陈灵  邹玉莲  黄秀旺  许建华
作者单位:1. 福建医科大学,药学院 福州,350122;2. 福建医科大学,免疫治疗研究所 福州,350122
基金项目:福建省自然科学基金,福建医科大学苗圃基金
摘    要:目的 观察雷公藤内酯醇(TPL)对肝癌H22细胞增殖、凋亡及环氧合酶-2(COX-2)表达水平的影响. 方法 以体外培养的鼠源性H22细胞株为研究对象,实验分对照组和不同浓度的TPL处理组.MTT比色法测定TPL对H22细胞株增殖抑制情况;TPL处理48 h后,Annexin V-FITC/PI双标记流式细胞术检测细胞凋亡情况,流式细胞术间接免疫荧光双标记法检测COX-2表达变化情况. 结果 随着药物浓度的增加及时间的延长,TPL能明显抑制H22细胞增殖.TPL诱导细胞凋亡及下调COX-2的表达具有浓度依赖性,不同浓度组比较,差别具有统计学意义(P<0.05). 结论 TPL可能通过诱导肝癌H22细胞凋亡及抑制COX-2表达发挥抗肿瘤作用.

关 键 词:雷公藤内酯  肝肿瘤  细胞凋亡  前列腺素内过氧化物合酶类

Effects of Triptolide on Proliferation, Apoptosis, and Cycloxygenase-2 Expressionin Hepatic Cancer Cell Line H22
GAN Chenling,ZOU Yulian,HUANG Xiuwang,XU Jianhua. Effects of Triptolide on Proliferation, Apoptosis, and Cycloxygenase-2 Expressionin Hepatic Cancer Cell Line H22[J]. Journal of Fujian Medical University, 2017, 51(3): 146-149
Authors:GAN Chenling  ZOU Yulian  HUANG Xiuwang  XU Jianhua
Affiliation:1. School of Pharmacy, Fujian Medical University, Fuzhou 350122, China;2. Institute of Immunotherapy, Fujian Medical University, Fuzhou 350122, China
Abstract:Objective To investigate the effects of triptolide (TPL) on proliferation, apoptosis, and cycloxygenase-2 (COX-2) expression in liver cancer line H22 and explore its anti-tumor mechanism.Methods H22 cultured in vitro was treated with different concentrations of triptolide, cell proliferation activity was determined by MTT assay.The Annexin V-FITC/PI cell apoptosis and COX-2 expression were assessed at 48 h after the onset of drug treatment by flow cytometry.Result Triptolide significantly inhibited the proliferation of H22 cells in a dose-and time-dependent manner.In addition, triptolide significantly induced cell apoptosis and down-regulated COX-2 expression in a dose-manner during 48 h.Conclusion TPL may play an anti-liver cancer role by inducing cell apoptosis and inhibiting COX-2 expression in H22 cells.
Keywords:triptolide  liver neoplasms  apoptosis  prostaglandin|endoperoxide synthases
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