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当前位置: 首页 > 文章 > 氯化钴诱导HepG2细胞低氧应激模型的建立 黑龙江八一农垦大学学报 2017 (4) 28-32
Position: Home > Articles > Establishment of Hypoxia Stress Model Using Cobalt Dichloride in HepG2 Cells Journal of Heilongjiang Bayi Agricultural University 2017 (4) 28-32

氯化钴诱导HepG2细胞低氧应激模型的建立

作  者：
常晓翠;范威锋;沈欢欢;黄向月;王升;王媛;冉伟;孙可新;姜楠;孔凡志
单  位：
大庆市人民医院检验科;黑龙江八一农垦大学动物科技学院
关键词：
氯化钴;低氧应激;腺苷酸激酶;低氧诱导因子
摘  要：
探索氯化钴(CoCl_2)诱导人肝癌细胞系HepG2建立低氧应激模型的条件,并评价该模型。不同浓度氯化钴处理HepG2细胞后,PCR法检测低氧诱导因子1α(HIF-1α)、激活转录因子4(ATF4)、腺苷酸激酶4(AK4)基因的表达;细胞计数法绘制对照组细胞和氯化钴处理组细胞的增殖曲线。随着CoCl_2浓度升高和处理时间的延长,HIF-1αm RNA和ATF4 m RNA表达显著升高、AK4 m RNA表达显著下降、HepG2细胞增殖速度显著下降(P<0.05)、细胞膜不完整边界不清。氯化钴化学模拟低氧过程中影响了缺氧主要调节因子HIF-1α的水平,因此以氯化钴用于构建模拟HepG2细胞缺氧诱导模型是可行的,ATF4和AK4可能在参与HepG2细胞抗低氧应激反应中起关键作用。此模型的建立为进一步研究AK4基因的生理学功能奠定了基础。
译  名：
Establishment of Hypoxia Stress Model Using Cobalt Dichloride in HepG2 Cells
作  者：
Chang Xiaocui;Fan Weifeng;Shen Huanhuan;Huang Xiangyue;Wang Sheng;Wang Yuan;Ran Wei;Sun Kexin;Jiang Nan;Kong Fanzhi;College of Animal Science and Veterinary Medicine,Heilongjiang Bayi Agricultural University;Laboratory Department,People's Hospital of Daqing;
关键词：
cobalt dichloride;;hypoxia stress;;adenylate kinase;;hypoxia induced factor
摘  要：
To find a proper condition to establish hypoxia stress model using cobalt dichloride in HepG2 cells and evaluate it.After using different concentration of CoCl_2 to treat HepG2 cells,expression of AK4,ATF4 and HIF-1α was detected by PCR;compare cell proliferation rate by cell counting. With the increase of CoCl_2,the expression of HIF-1α m RNA and ATF4 m RNA were both increased,however,AK4 m RNA were decreased significantly;cell proliferation rate was decreased significantly(P <0.05)and the membrane was broken. The expression of HIF-1α,which was the most important transcription factor in hypoxia stress,were increased in HepG2 cells during CoCl_2 treatment,so,it was feasible to establish hypoxia stress model by using CoCl_2. ATF4 and AK4 may play an important role in protecting HepG2 cells from hypoxia stress. Establishment of this model may lay a foundation for further research on AK4 physiology function.

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