新疆大学生命科学与技术学院新疆生物资源基因工程重点实验室
纸质出版:2022
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[1]夏丽洁,迪丽尼格尔·孜亚依丁,魏仙仙,等.中亚苦蒿醇提物诱导人食管癌细胞凋亡及其作用机制的研究[J].新疆大学学报(自然科学版)(中英文),2022,39(04):462-469+475.
[1]夏丽洁,迪丽尼格尔·孜亚依丁,魏仙仙,等.中亚苦蒿醇提物诱导人食管癌细胞凋亡及其作用机制的研究[J].新疆大学学报(自然科学版)(中英文),2022,39(04):462-469+475. DOI: 10.13568/j.cnki.651094.651316.2021.09.30.0003.
DOI:10.13568/j.cnki.651094.651316.2021.09.30.0003.
为探究中亚苦蒿大孔树脂85%乙醇洗脱相(85%ethanol elution fraction of Artemisia absinthium L. ethanol extract with macroporous resin
AEMV)诱导食管癌Eca109细胞凋亡的作用机制,采用MTT法检测AEMV体外对人食管癌Eca109细胞增殖的影响,流式细胞术检测细胞周期变化和凋亡率,Western Blot检测相关通路蛋白的表达变化.研究结果表明:与对照DMSO组相比,AEMV可以浓度依赖性显著抑制Eca109细胞的增殖(P <0.001)
IC50值为57.76μg/mL
AEMV可诱导Eca109细胞凋亡(P <0.001)和染色质固缩.通过下调cyclin B1的表达,50μg/mL AEMV阻滞细胞周期在G0/G1期,100μg/mL AEMV可将细胞周期阻滞于G2/M期.同时,100μg/mL AEMV通过诱导胞内活性氧水平提高(P <0.001)、线粒体膜电位下降(P <0.001),剂量依赖性地增加caspase-9、caspase-3和PARP的剪切,激活线粒体内源caspase依赖凋亡途径.还发现AEMV能够激活Eca109细胞的内质网应激(ER stress),上调ER stress通路相关蛋白GRP78、p-PERK、p-eIF-2α和CHOP的表达.综上,AEMV通过线粒体依赖和内质网应激途径诱导Eca109细胞凋亡,提示AEMV可能是治疗食管癌的潜在候选药物.
To investigate the mechanism of cell apoptosis in human esophageal carcinoma cells Eca109 induced by 85% ethanol elution fraction of Artemisia absinthium L. extract with macroporous resin(AEMV)
in this study
the effect on the proliferation of Eca109 cells induced by AEMV was detected by MTT assay in vitro. Flow cytometry was used to detect the change of cell cycle and apoptosis ratio. The change of related proteins expression was detected by Western Blot. The results showed that AEMV could significantly inhibit cell proliferation in a concentration dependent manner
which compared with the DMSO group(P <0.001). The IC50 is 57.76 μg/mL.AEMV could induce apoptosis(P <0.001) and chromatin condensation of Eca109 cells. The cell cycle was arrested by down regulating the expression of cyclin B1. 50 μg/mL AEMV induced arrest cell cycle at the G0/G1 phase
100 μg/mL AEMV induced cell cycle arrest at the G2/M phase. 100 μg/mL AEMV can increase the level of intracellular reactive oxygen species(P <0.001)
decrease the mitochondrial membrane potential(P <0.001) and activate the mitochondrial-mediated intrinsic caspase-dependent pathway by increasing the expression of cleaved caspase-9
caspase-3 and PARP in a dose-dependent manner. This study also found that AEMV could activate endoplasmic reticulum stress(ER stress) in Eca109 cells by up regulating the expression of GRP78
p-PERK
p-eIF-2α and CHOP. In conclusion
AEMV induces ROS production
activates endoplasmic reticulum stress and induces apoptosis of Eca109 cells through mitochondrial-mediated intrinsic caspase-dependent pathway. It is suggested that AEMV may be a potential candidate drug for the treatment of esophageal carcinoma.
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