β-榄香烯阻断JAK2-STAT3信号通路促进紫杉醇对肺癌细胞增殖和凋亡作用研究  

Blockade of JAK2-STAT3 Signaling Pathway by β-elemene Promoting Proliferation and Apoptosis of Lung Cancer Cells by Paclitaxel

作　　者：王峥嵘[1] 范焕芳[1] 张倩 郭洁[3] 李德辉[1] WANG Zhengrong;FAN Huanfang;ZHANG Qian;GUO Jie;LI Dehui(Tumor Department Two,Hebei Provincial Hospital of Traditional Chinese Medicine,Shijiazhuang 050051,Hebei,China;Respiratory Department,Hebei Provincial Hospital of Traditional Chinese Medicine,Shijiazhuang 050051,Hebei,China;Surgery Department Two,Xinle Hospital,Xinle 050700,Hebei,China)

机构地区：[1]河北省中医院肿瘤二科,河北石家庄050051 [2]新乐市医院外二科,河北新乐050700 [3]河北省中医院呼吸二科,河北石家庄050051

出　　处：《中华中医药学刊》2019年第7期1600-1604,共5页Chinese Archives of Traditional Chinese Medicine

基　　金：国家自然科学基金项目(81603412)

摘　　要：目的:研究分析讨论β-榄香烯对紫杉醇抑制肺癌细胞增殖、诱导凋亡的作用,并探讨其可能的机制。方法:建立耐药细胞株A549/Taxol,MTT法测定β-榄香烯对A549/Taxol细胞株的抑制率及IC50;使用Annexin V-FITC/PI检测细胞凋亡率;并通过Western Blot法检测JAK2、STAT3、p-STAT3、Bcl-2、Bax、Caspase3蛋白的表达水平,借以分析β-榄香烯对紫杉醇抑制肺癌细胞增殖、诱导凋亡的作用和机制。结果:药物干预48 h后,可见β-榄香烯对A549/Taxol肺癌细胞活性均显示出抑制作用,并且抑制作用表现出明显的剂量依赖性,对肺癌细胞抑制的IC50水平为108.5μg/mL。研究中采用IC50浓度108.5μg/mL榄香烯干预A549/Taxol肺癌细胞, 24 h后可见A549/Taxol肺癌细胞的凋亡水平显著增加(P<0.05);与此同时,肺癌细胞JAK2、STAT3、p-STAT3和Bcl-2可见降低(P<0.05),而Bax和Caspase3则见升高(P<0.05)。结论:β-榄香烯可能通过抑制JAK2/STAT3信号通路,发挥拮抗肺癌细胞对紫杉醇的耐药性作用,抑制肿瘤细胞增殖,诱导凋亡。Objective: To investigate the effect of β-elemene on paclitaxel inhibition of lung cancer cell proliferation and induction of apoptosis and explore its possible mechanism. Methods:A549/Taxol was established in the study. The inhibition rate and IC50 of β-elemene on A549/Taxol cell line were determined by MTT assay. Apoptosis rate was detected by Annexin V-FITC/PI. Western blot was used. The expression levels of JAK2, STAT3, p-STAT3, Bcl-2, Bax and Caspase3 were detected to analyze the effect and mechanism of β-elemene on paclitaxel inhibiting proliferation and inducing apoptosis of lung cancer cells. Results:After 48 h of drug intervention,β-elemene showed inhibition of A549/Taxol lung cancer cell activity, and the inhibitory effect showed a dose-dependent effect. The IC50 level of inhibition of lung cancer cells in this study was 108.5 μg/mL. In the study, the A549/Taxol lung cancer cells were treated with IC50 concentration of 108.5 μg/mL elemene. After 24 h, the apoptosis level of A549/Taxol lung cancer cells was significantly increased(P<0.05). At the same time, lung cancer cells JAK2, STAT3, p-STAT3 and Bcl-2 were decreaed(P<0.05), while those of Bax and Caspase3 were increased(P<0.05). Conclusion:β-elemene may inhibit the drug resistance of lung cancer cells to paclitaxel by inhibiting JAK2/STAT3 signaling pathway, inhibiting tumor cell proliferation and inducing apoptosis.

关 键 词：Β-榄香烯 JAK2-STAT3信号通路 紫杉醇 增殖 凋亡 

分 类 号：R285.5[医药卫生—中药学]