蒲公英萜醇对乳腺癌细胞增殖及发生氧化应激反应的影响
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摘要
目的 :探究蒲公英萜醇(Taraxerol)对乳腺癌细胞(MCF-7细胞)增殖及发生氧化应激反应的影响。方法 :将MCF-7细胞接种于96孔板中,在其中4孔的MCF-7细胞中分别加入12.5μmol/L、25μmol/L、50μmol/L、100μmol/L和200μmol/L的蒲公英萜醇,对其中一孔的MCF-7细胞不进行添加蒲公英萜的处理。将未经处理的MCF-7细胞设为对照组(Control组),将其他的MCF-7细胞设为用药组。采用细胞计数试剂盒(cell counting kit-8,CCK-8)检测加入不同浓度的蒲公英萜醇对各用药组细胞增殖的影响,采用探针DCFH-DA检测各组细胞中活性氧(ROS)的变化,采用分光光度法测定各组细胞中上清液乳酸脱氢酶(LDH)及细胞中丙二醛(MDA)、超氧化物歧化酶(SOD)含量。结果 :进行CCK-8检测的结果显示,在各用药组细胞中加入蒲公英萜醇后的第48 h和第72 h其增殖速度均明显下降,与对照组细胞相比差异有统计学意义,P<0.05。与对照组细胞相比,各用药组细胞中ROS、LDH、MDA的水平均明显上升(P<0.05),其中SOD的水平均明显下降(P<0.05),且在各用药组细胞中加入蒲公英萜醇的浓度越高,其ROS、LDH、MDA、SOD水平的变化幅度越大。结论 :蒲公英萜醇可抑制乳腺癌细胞MCF-7细胞的增殖,其作用机制可能与其能够诱导该细胞发生氧化应激性损伤有关。
Objective: To investigate effect of Taraxerol to proliferation and oxidative stress of MCF-7 cells.Methods: Inoculate MCF-7 cells into 96-well plates, respectively drop concentration of 25 umol/L,50 umol/L,100 umol/L,200 umol/L of Taraxerol for each 4 wells on the plate, but leave one well without Taraxerol. Set the well of MCF-7 cells without Taraxerol to control group, set the wells of MCF-7 cells with Taraxerol to experimental group. Apply cell counting kit-8(CCK-8)to test effect of Taraxerol in different concentration to proliferation of each group of the cells, apply probe DCFH-DA to test ROS variation of each group of the cells, apply spectrophotometry to test LDH, MDA and SOD content of each group of the cells.Results: The result of CCK-8 shows that in 48 th hour and 72 th hour proliferation speed of MCF-7 cells in experimental significantly slower than control group(P <0.05).Compare with control group, ROS,LDH and MDA level of experimental group are significantly increased(P <0.05)but SOD level significantly decreased. The change range of ROS,LDH,MDA and SOD level of MCF-7 cells will become larger with concentration of Taraxerol increasing. Conclusion: Taraxerol have a inhibition effects of MCF-7 cells,the mode of action of Taraxerol may related with oxidative stress of MCF-7 cells.
Objective: To investigate effect of Taraxerol to proliferation and oxidative stress of MCF-7 cells.Methods: Inoculate MCF-7 cells into 96-well plates, respectively drop concentration of 25 umol/L,50 umol/L,100 umol/L,200 umol/L of Taraxerol for each 4 wells on the plate, but leave one well without Taraxerol. Set the well of MCF-7 cells without Taraxerol to control group, set the wells of MCF-7 cells with Taraxerol to experimental group. Apply cell counting kit-8(CCK-8)to test effect of Taraxerol in different concentration to proliferation of each group of the cells, apply probe DCFH-DA to test ROS variation of each group of the cells, apply spectrophotometry to test LDH, MDA and SOD content of each group of the cells.Results: The result of CCK-8 shows that in 48 th hour and 72 th hour proliferation speed of MCF-7 cells in experimental significantly slower than control group(P <0.05).Compare with control group, ROS,LDH and MDA level of experimental group are significantly increased(P <0.05)but SOD level significantly decreased. The change range of ROS,LDH,MDA and SOD level of MCF-7 cells will become larger with concentration of Taraxerol increasing. Conclusion: Taraxerol have a inhibition effects of MCF-7 cells,the mode of action of Taraxerol may related with oxidative stress of MCF-7 cells.
引文
[1]Torre LA,Bray F,Siegel RL,Ferlay J,Lortet-Tieulent J,Jemal A.Global cancer statistics,2012.CA Cancer J Clin.2015;65(2):87-108.
[2]Sharma K.,R.Zafar.Occurrence of taraxerol and taraxasterol in medicinal plants[J].Pharmacogn Rev,2015,9(17):19-23.
[3]谭宝,石海莲,季光,等.蒲公英萜醇和乙酰蒲公英萜醇对胃癌细胞株AGS细胞周期和凋亡的影响[J].中西医结合学报,2011(6):638-642.
[4]LI SA,SHI Y,SHANG XY,et al.Triter penoids from the roots of P terospermum heterophy llum Hance[J]..J Asian Nat Prod Res.2009;11(7):652-657.DOI:10.1080/10286020902964248.
[5]DING Y,WANG H,NIU J,et al.Induction of ROS overload by al antolactone prompts oxidative DNA damage and apoptosis.in co lorectal cancer cells[J].Int J Mol Sci,2016,17(4).pii:E558.doi:10.3390/ijms17040558.
[6]ZHU B,LI Y,LIN Z,et al.Silver nanoparticles induce He PG-2cells apoptosis through ROS-mediated signaling pathways[J].Nanoscale Res Lett,2016,11(1):198.
[7]皇甫冰,高继萍,杨霞,等.氧化应激与肾脏细胞凋亡[J].中国比较医学杂志,2015,25(2):54-60.
[2]Sharma K.,R.Zafar.Occurrence of taraxerol and taraxasterol in medicinal plants[J].Pharmacogn Rev,2015,9(17):19-23.
[3]谭宝,石海莲,季光,等.蒲公英萜醇和乙酰蒲公英萜醇对胃癌细胞株AGS细胞周期和凋亡的影响[J].中西医结合学报,2011(6):638-642.
[4]LI SA,SHI Y,SHANG XY,et al.Triter penoids from the roots of P terospermum heterophy llum Hance[J]..J Asian Nat Prod Res.2009;11(7):652-657.DOI:10.1080/10286020902964248.
[5]DING Y,WANG H,NIU J,et al.Induction of ROS overload by al antolactone prompts oxidative DNA damage and apoptosis.in co lorectal cancer cells[J].Int J Mol Sci,2016,17(4).pii:E558.doi:10.3390/ijms17040558.
[6]ZHU B,LI Y,LIN Z,et al.Silver nanoparticles induce He PG-2cells apoptosis through ROS-mediated signaling pathways[J].Nanoscale Res Lett,2016,11(1):198.
[7]皇甫冰,高继萍,杨霞,等.氧化应激与肾脏细胞凋亡[J].中国比较医学杂志,2015,25(2):54-60.