丹皮酚抑制GLC-82细胞增殖的体外实验研究  被引量:8

In Vitro Study of the Anti-proliferative and Apoptotic Effects of Paeonol on the GLC-82 Cells

在线阅读下载全文

作  者:张旃[1] 李明昌[2] 谭炳炎[3] 欧阳丽萍[3] 陆家海[3] 罗斌[2] 

机构地区:[1]广东省第二人民医院呼吸内科,广州510310 [2]广州医学院第二附属医院神经外科,广州510260 [3]中山大学公共卫生学院,广州510080

出  处:《热带医学杂志》2006年第6期638-640,637,F0004,共5页Journal of Tropical Medicine

基  金:广东省中医药管理局资助课题(No.103104);广州市卫生局中西医结合课题(No.2005A065);广州医学院博士启动基金(No.04-G-12)

摘  要:目的探讨丹皮酚(paeonol,Pae)对人肺癌细胞株GLC-82增殖和凋亡的影响。方法采用MTT法检测丹皮酚对体外培养的人肺癌细胞株GLC-82的增殖抑制作用,用透射电镜和流式细胞仪观察Pae对GLC-82细胞的诱导凋亡作用。结果Pae在31.25~250mg/L浓度范围内对GLC-82细胞的增殖均有抑制作用,呈现明显的量效和时效依赖关系。透射电镜下可见肿瘤细胞发生凋亡改变。Pae在31.25~250mg/L浓度下均可诱导GLC-82细胞发生凋亡,有明显的时效和量效关系。丹皮酚作用后细胞周期发生明显变化,主要表现为S期细胞增加,G0/G1期和G2/M期细胞减少,细胞周期几乎停滞于S期。结论Pae有抑制人肺癌细胞株GLC-82的增殖和诱导其发生凋亡的作用。Objective To investigate the in vitro effect of paeonol on proliferation and apoptosis of GLC-82. Method The inhibitory effect of paeonol on the proliferation of GLC-82 ceils was assayed by MTT method; the morphology of apoptotic cells was observed by transmission electron microscope; flow cytometry was used to analyze the apeptosis of GLC-82 cells induced by paeonol, Result The proliferation of GLC-82 cells was inhibited by paeonol with the concentration of 31.25 mg/L to 250 mg/L in dose and time dependent manner. Typical apoptotic changes in GLC-82 ceils were observed by transmission electron microscope. The apoptotic rates of GLC-82 ceils were increased when the concentrations of paeonol increased from 31.25 mg/L to 250 mg/L, which also showed obvious time effect relationship. The distribution of ceil cycle was also changed after treated by paeonol, The number of ceils in S phase was increased and that in G0/G1 phase and G2/M phase were decreased and the ceil cycle was arrested in S phase. Conclusion Paeonol can inhibit the proliferation and induce apoptosis of GLC-82 ceils.

关 键 词:丹皮酚 肺癌 增殖 凋亡 

分 类 号:R734.2[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象