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作 者:任开明[1] 周兆丽 石文君[1] REN Kai-ming;ZHOU Zhao-li;SHI Wen-jun(Department of Thoracic Surgery, Shengjing Hospital of China Medical University, Shenyang 110001, China;Department of Pharmacology, Shanghai University of Medicine & Health Sciences, Shanghai 20131, China)
机构地区:[1]中国医科大学附属盛京医院胸外科,辽宁沈阳110004 [2]上海健康医学院药理教研室,上海201318
出 处:《解剖科学进展》2019年第4期361-363,367,共4页Progress of Anatomical Sciences
基 金:国家自然科学基金青年基金(81803581)
摘 要:目的探讨木犀草素对非小细胞肺癌A549细胞增殖、凋亡、侵袭及迁移能力的影响及可能机制。方法分别采用0、20、40、60μmol/L的木犀草素与非小细胞肺癌A549细胞共同培养,MTT法检测A549细胞在培养0、24、48、72h时细胞的生存率。40μmol/L木犀草素与A549细胞共同培养48h后,流式细胞仪检测细胞凋亡能力的变化;Transwell实验检测细胞侵袭、迁移能力;WesternBlot方法检测A549细胞Caspase-3、p-Akt、基质金属蛋白酶2、9(MMP2、MMP9)的蛋白表达变化。结果20、40、60μmol/L木犀草素均能够显著抑制A549细胞的增殖,抑制效果具有药物浓度和时间依赖性。与对照组比较,40μmol/L木犀草素能够显著促进A549细胞的凋亡,抑制A549细胞的侵袭与迁移,上调Caspase-3的表达,抑制p-Akt、MMP2与MMP9的蛋白表达(P<0.05)。结论木犀草素抑制A549细胞增殖、侵袭及迁移能力,诱导细胞凋亡,与上调Caspase-3的表达并抑制p-Akt、MMP2与MMP9的表达相关。Objective To investigate the effects of luteolin on proliferation, apoptosis, invasion and migration of human non-small cell lung cancer A549 cells. Methods Luteolin at 0, 20, 40 and 60μmol/L was co-cultured with nonsmall cell lung cancer A549 cells. The survival rate of A549 cells at 0, 24, 48 and 72 h was detected by MTT method. 48 h after luteolin and A549 cells were co-cultured, flow cytometry was used to detect the changes of apoptotic ability;Transwell assay was used to detect the invasion and migration ability of A549 cells;Western blot was used to detect the expression of Caspase-3, p-Akt, matrix metalloproteinase-2, 9(MMP-2, MMP-9) in A549 cells. Results Luteolin at 20, 40 and 60 μmol/L significantly inhibited the proliferation of A549 cells with time-dependent and concentration-dependent manner. Compared with the control group, 40 micromol/L luteolin promoted significantly A549 cells apoptosis, and inhibited the invasion and migration of A549 cells, up-regulated the expression level of Caspase-3, and inhibited the expression levels of p-Akt, MMP2 and MMP9 proteins(P<0.05). Conclusion Luteolin inhibited the proliferation, invasion and migration of A549 cells and induced apoptosis, which is related to up-regulation of Caspase-3 expression and inhibition of p-Akt, MMP2 and MMP9 expression.
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