摘要
目的:研究牡丹苷A对人肺癌A549细胞株的作用以及其诱导人肺癌A549细胞株凋亡机制。方法:本研究采用MTT法检测牡丹苷A对体外人肺癌细胞株A549增殖率的影响。Annexin V/PI双标法检测牡丹苷A对A549凋亡率,蛋白免疫印迹法和细胞免疫细胞化学法分别检测牡丹苷A对A549细胞株PI3K,Akt,NF-κBp65,Bax,Bcl-2的表达,并采用PI3K/Akt/NF-κB通路的激动剂IGF-1和抑制剂wortmannin进一步探讨牡丹苷A对PI3K/Akt/NF-κB信号通路的作用。结果:牡丹苷A能够抑制A549的增殖,上调Bax蛋白的表达量,下调Bcl-2蛋白的表达量,Bcl-2/Bax比值显著降低,同时降低PI3K,NF-κBp65的蛋白表达,抑制Akt磷酸化。结论:牡丹苷A能够阻碍A549增殖,并促进其凋亡,其诱导凋亡的机制可能与抑制PI3K/Akt/NF-κB通路有关。
OBJECTIVE To observe effects and mechanism of suffruticoside A （SCA） to induce apoptosis of human lung cancer cell line A549.METHODS MTT assay was used to detect proliferation of A549 cells by SCA treatment. Besides, apoptosis of A549 was tested by Annexin V/PI method. Immunocytochemistry （IHC） and western blot （WB） were applied for evaluation of PI3K, Akt, NF-κBp65, Bax and Bcl-2 expressions, respectively. Insulin-like growth factor-1（IGF-1, one of the most potent activators of PI3K/Akt signaling pathway） and wortmannin （a strong PI3K/Akt inhibitor） were used to evaluate underlying mechanisms.RESULTS SCA was beneficial to inhibit proliferation of A549 cells. Apoptosis of A549 tested by Annexin V/PI method showed effects of SCA on promoting A549 apoptosis. Expression of Bax protein was up-regulated, whereas expression of PI3K, NF-κBp65 and Bcl-2 proteins were down-regulated by SCA. Phosphorylation of NF-κBp65 was inhibited after treatment of SCA. Ratio of Bcl-2/Bax was significantly reduced, indicating that SCA could induce apoptosis of A549 tumor cells.CONCLUSION SCA can inhibit A549 proliferation and induce apoptosis, and mechanism to induce apoptosis may be related to inhibition of PI3K/Akt/NF-κB pathway.
出处
《中国医院药学杂志》
CAS
CSCD
北大核心
2016年第12期993-998,共6页
Chinese Journal of Hospital Pharmacy
