外源性类活性氧诱导直肠癌细胞凋亡的机制

The Effects of Exogenous Reactive Oxygen Species (HClO) on Rectal Cancer Cells

目的:探究类活性氧HClO诱导正常细胞和直肠癌细胞凋亡的潜在机制。方法:用不同浓度的次氯酸干预内皮细胞Ealy926和直肠癌细胞HCT-8,通过MTT法检测细胞增殖率;吉姆萨染色法观察细胞形态学变化;流式细胞术检测细胞的凋亡率。结果:MTT结果显示HClO抑制Ealy926和HCT-8的增殖(P均<0.05),呈浓度依赖性;吉姆萨染色显示,Ealy926和HCT-8细胞经不同浓度HClO干预后细胞的形态学发生明显的变化,如细胞皱缩、细胞核边缘化、细胞碎裂等;流式细胞术检测结果显示,HClO使内皮细胞Ealy926和直肠癌细胞HCT-8的凋亡率增加(P均<0.05),呈浓度依赖性。结论:添加外源性类活性氧(HClO)能够抑制内皮细胞Ealy926和直肠癌细胞HCT-8增殖,诱导细胞内ROS释放,造成细胞的氧化损伤,使细胞凋亡,高浓度直接导致细胞坏死。分析结果发现直肠癌细胞HCT-8对类活性氧HClO的敏感性高于内皮细胞Ealy926。

Objective:To investigate the potential mechanism of reactive oxygen species HClO-induced apoptosis in normal and rectal cancer cells.Methods:Endothelial cells Ealy926 and rectal cancer cell HCT-8 were treated with different concentrations of hypochlorous acid.Cell proliferation was detected by MTT assay.Cell morphology was observed by Giemsa staining.Apoptosis rate was detected by flow cytometry.Results:MTT assay showed that HClO inhibited the proliferation of Ealy926 and HCT-8 in a concentration-dependent manner(P<0.05).Giemsa staining showed that the morphology of endothelial cells Ealy926 and rectal cancer cell HCT-8 were significantly changed after different concentrations of HClO,such as cell shrinkage,nuclear marginalization,cell fragmentation,etc.The results of cytometry showed that HClO increased the ROS of endothelial cells Ealy926 and rectal cancer cells HCT-8 in a concentration-dependent manner,and the apoptotic rate increased(P<0.05).Conclusion:The addition of exogenous reactive oxygen species(HClO)can inhibit the proliferation of endothelial cells Ealy926 and rectal cancer cells HCT-8,induce the release of intracellular ROS,cause oxidative damage of cells,and cause apoptosis.High concentration directly leads to cell necrosis.The analysis found that rectal cancer cell HCT-8 is more sensitive to reactive oxygen species HClO than endothelial cell Ealy926.