郭立彬 董秋峰 付宏亮 仼红刚 刘跃亭.beta榄香烯对人脑胶质瘤SHG44 细胞增殖及凋亡的影响[J].,2016,16(6):1039-1042 |
beta榄香烯对人脑胶质瘤SHG44 细胞增殖及凋亡的影响 |
Effects of beta-Elemene on the Proliferation and Apoptosis of SHG44 HumanGlioma Cells |
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DOI: |
中文关键词: beta- 榄香烯 胶质瘤 SHG44 Bcl-2 Bax |
英文关键词: beta-Elemene Glioma SHG44 Bcl-2 Bax |
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中文摘要: |
目的:探讨中药提取物beta- 榄香烯对胶质瘤SHG44 细胞增殖抑制作用及对Bax 和Bcl-2 蛋白表达的影响,并进一步探讨发
生的机制。方法:用不同浓度的beta-榄香烯对体外培养的SHG44 细胞进行干预,分别采用MTT、流式细胞仪检测法,观察beta-榄香
烯对SHG44细胞增殖的抑制和凋亡诱导作用,并通过Western blot检测凋亡相关蛋白Bax 与Bcl-2 蛋白表达情况。结果:经beta-
榄香烯处理SHG44细胞后,MTT 结果其发现SHG44细胞生长受药物浓度和时间的影响,细胞生长明显被抑制,且(P<0.05),流
式细胞术显示,茁- 榄香烯诱导SHG44细胞后,细胞凋亡指数伴随药物作用时间的延长凋亡显著增加;Western blot 结果发现,beta-
榄香烯对SHG44 细胞的诱导后,使促凋亡蛋白Bax 和抑凋亡蛋白Bcl-2 与对照组相比发生了显著改变,且实验组Bax 蛋白表达
明显高于对照组,而抑凋亡蛋白Bcl-2 的表达伴随beta- 榄香烯的作用时间的增加,表达也逐渐减少。结论:beta- 榄香烯能显著抑制胶
质瘤SHG44 细胞的增殖,促进其凋亡;其机制可能与调控Bcl-2 和Bax表达有关。 |
英文摘要: |
Objective:To investigate the effects of beta-Elemene, one traditional Chinese medicine extract, on cell proliferation in
glioma SHG44 cells and its underlying mechanisms.Methods:Glioma SHG44 cells were treated by beta-Elemene with different
concentrations in vitro, and the effects on cell proliferation and apoptosis were detected by MTT assay and flow cytometry respectively.
Western blotting was further performed to analyze the influences on protein expression of Bax and Bcl-2, two of apoptosis-related
proteins.Results:As MTT results showed, SHG44 cell viability was significantly suppressed by beta-Elemene in a time- and
concentration-dependent manner (P<0.05). Results from flow cytometry indicated that beta-Elemene induced remarkable apoptosis in
SHG44 cells as treatment prolonged. In addition, the influences of beta-Elemene on protein expression of Bax and Bcl-2 were confirmed by
Western blotting, showing a time-dependent increase in the expression of Bax and decrease in expression of Bcl-2 following beta-Elemene
treatment.Conclusion:beta-Elemene exhibits remarkable potential to inhibit cell proliferation, and induce apoptosis in glioma SHG44 cells.
The underlying mechanisms may be related to its regulation on the expression of Bax and Bcl-2. |
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