论文部分内容阅读
目的:研究内毒素对体外培养非小细胞肺癌(NSCLC)细胞株A549细胞增殖的影响及其机制。方法:不同浓度脂多糖(LPS)进行8-48h干预,MTT及细胞计数法检测其对A549细胞增殖的影响;EGFR中和抗体或COX-2抑制剂与LPS联合干预,检测其对A549细胞增殖及PGE2的影响。结果:LPS可引发A549细胞MTT活性和细胞计数显著增加,且呈现时间和剂量依赖性。LPS还可诱发PGE2水平显著升高。药物干预结果显示,抑制COX-2或EGFR可明显逆转LPS所引发的细胞增殖和PGE2水平升高趋势。结论:LPS可能通过激活EGFR和COX-2信号途径,诱导体外培养的非小细胞肺癌细胞增殖分化。肺部感染可能会加速非小细胞肺癌进展,并可能造成不良预后。
Objective: To study the effect of endotoxin on the proliferation of non-small cell lung cancer (NSCLC) cell line A549 and its mechanism. Methods: Interfering with different concentrations of lipopolysaccharide (LPS) for 8-48h, MTT and cell counting were used to detect the effect of LPS on the proliferation of A549 cells. EGFR neutralizing antibody or COX-2 inhibitor was used in combination with LPS to detect the proliferation of A549 cells And PGE2 effects. Results: LPS induced a significant increase in MTT activity and cell count of A549 cells in a time and dose dependent manner. LPS can also induce a significant increase in PGE2 levels. Drug intervention results show that inhibition of COX-2 or EGFR can significantly reverse the LPS-induced cell proliferation and PGE2 levels increased. Conclusion: LPS may induce the proliferation and differentiation of non-small cell lung cancer cells by activating EGFR and COX-2 signaling pathways. Pulmonary infection may speed up the progression of non-small cell lung cancer and may cause poor prognosis.