CAJ | 학술논문

目的探讨褪黑素( Mel)对人肺腺癌A549细胞增殖的影响及其作用机制。方法以人肺腺癌细胞株A549为研究对象，分别用不同浓度的Mel处理A549细胞，用四甲基偶氮唑蓝( MTT)法检测Mel对A549细胞增殖的影响；光学显微镜下观察 A549细胞形态学变化；Western blot 分析细胞MAPK信号通路相关蛋白及骨桥蛋白( OPN)表达的变化。结果Mel对A549细胞有明显的增殖抑制作用，并呈浓度和时间依赖性；高浓度(2.0 mmol/L) Mel处理组A549细胞数量减少，形态由梭形变成不规则形，细胞间间隙明显增大，成单层生长；Western blot检测显示2.0 mmol/L浓度的Mel能显著抑制JNK、p38的磷酸化，而使ERK磷酸化水平增加；同时，该浓度的Mel能明显抑制OPN蛋白的表达。结论 Mel能够呈浓度、时间依赖性抑制 A549细胞的增殖，调节MAPK信号通路磷酸化水平和抑制OPN的表达可能为其作用路径之一。
목적탐토퇴흑소( Mel)대인폐선암A549세포증식적영향급기작용궤제。방법이인폐선암세포주A549위연구대상，분별용불동농도적Mel처리A549세포，용사갑기우담서람( MTT)법검측Mel대A549세포증식적영향；광학현미경하관찰 A549세포형태학변화；Western blot 분석세포MAPK신호통로상관단백급골교단백( OPN)표체적변화。결과Mel대A549세포유명현적증식억제작용，병정농도화시간의뢰성；고농도(2.0 mmol/L) Mel처리조A549세포수량감소，형태유사형변성불규칙형，세포간간극명현증대，성단층생장；Western blot검측현시2.0 mmol/L농도적Mel능현저억제JNK、p38적린산화，이사ERK린산화수평증가；동시，해농도적Mel능명현억제OPN단백적표체。결론 Mel능구정농도、시간의뢰성억제 A549세포적증식，조절MAPK신호통로린산화수평화억제OPN적표체가능위기작용로경지일。
Objective To explore the effect of melatonin on the proliferation of human lung adenocarcinoma cells and its mechanism. Methods Regard lung adenocarcinoma cancer cell strains as the research object. The A549 cells were treated with different concentration of melatonin ( Mel) . The proliferation of A549 cells was observed by MTT assay. The change of cell morphology was observed by light microscope. The expression of MAPK related pro-tein and OPN was analyzed by Western blot. Results Mel could inhibit the proliferation of A549 cells in a dose-dependent and time-dependent manner. Compared with control group, A549 cells in the group treated with Mel be-came lesser, more irregular, bigger intercellular gap, non-overlapping and monolayer. The Western blot analysis il-lustrated that 2. 0mmol/L Mel could significantly decreased the expression of phosphorylation of JNK, p38 and OPN in A549 cells ( P<0 . 05 ) , and the expression of phosphorylation of ERK was increased ( P<0 . 05 ) , compared with control group. Conclusion Mel can inhibit the proliferation of A549 cells in a dose-dependent and time-de-pendent manner, which may be related to decrease the expression of OPN by regulating the phosphorylation level of MAPK signal pathway.