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探讨了双氢青蒿素联合吉非替尼对人非小细胞肺癌细胞(吉非替尼敏感细胞株PC-9和吉非替尼耐药细胞株H1975)的抑制效果及协同机制.运用噻唑蓝法和克隆形成实验,比较双氢青蒿素和吉非替尼单独给药和联合给药对肺癌细胞存活率和克隆形成能力的影响;利用Western blot检测单独给药和联合给药时EGFR信号通路和STAT3信号通路的变化.实验结果显示,双氢青蒿素和吉非替尼联合使用优于单独给药,联合用药指数值分别为0.751(PC-9细胞)和0.766(H1975细胞).吉非替尼诱导激活的STAT3反馈激活途径导致非小细胞肺癌对TKI产生耐药,双氢青蒿素可抑制吉非替尼激活的STAT3且不影响其TKI活性,提示双氢青蒿素可以作为解决TKI耐药的候选药物.
To investigate the inhibitory effect and synergistic mechanism of dihydroartemisinin and gefitinib on human non-small cell lung cancer cells (gefitinib sensitive cell line PC-9 and gefitinib resistant cell line H1975) Blue method and clonogenic assay were used to compare the effects of dihydroartemisinin and gefitinib on the survival rate and clonogenic capacity of lung cancer cells alone and in combination.Western blot was used to detect the effect of EGFR Signal pathways and STAT3 signal pathways.Experimental results show that the combination of dihydroartemisinin and gefitinib is superior to the single administration, the combined drug index values were 0.751 (PC-9 cells) and 0.766 (H1975 cells) Gefitinib induced activation of STAT3 feedback pathway lead to non-small cell lung cancer resistant to TKI, dihydroartemisinin can inhibit gefitinib-activated STAT3 and does not affect its TKI activity, suggesting that dihydroartemisinin Can be used as a drug candidate to solve TKI resistance.