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作 者:王盼[1] 白剑英[1] 梁瑞峰[1] 闫丹丹[1] 易鑫[1]
机构地区:[1]山西医科大学公共卫生学院环境卫生教研室,山西太原030001
出 处:《毒理学杂志》2017年第1期30-34,共5页Journal of Toxicology
基 金:山西省留学回国人员科技活动择优资助项目(2014-95);山西省自然科学基金(2013011052-1)
摘 要:目的探讨甲醛对HepG2细胞凋亡的影响。方法以0.004、0.02、0.1、0.5、2.5、12.5 mmol/L的甲醛(formaldehyde)分别处理人肝癌HepG2细胞24和48 h,采用MTT法检测细胞活性。分别以0.004、0.02、0.1 mmol/L的甲醛处理人肝癌HepG2细胞24和48 h,采用Western blot法检测p53、mdm2、Caspase-3、RIP1、RIP3和NF-κB的蛋白表达水平。结果与阴性对照组相比较,0.5~12.5 mmol/L FA染毒24和48 h可显著降低HepG2细胞活性(P<0.05);染毒24 h后Caspase-3蛋白表达降低(P<0.05);p53、p-p53、mdm2、RIP3表达水平在染毒24和48 h后均明显降低(P<0.05);cleaved RIP1表达水平在0.1 mmol/L剂量染毒24和48 h后表达增加(P<0.05)上述变化均有统计学意义;染毒24和48 h后NF-κB蛋白表达无明显变化。结论甲醛可能是通过死亡受体途径而不是线粒体途径引起肝细胞凋亡。Objective To investigate the effects and possible mechanism of formaldehyde on the apoptosis of HepG2 hepatocytes.Methods HepG2 cells were treated with formaldehyde at 0. 004,0. 02,0. 1,0. 5,2. 5 and 12. 5 mmol/L,MTT method was used to detect cell viability. The expression levels of p53,mdm2,Caspase-3,RIP1,RIP3 and NF-κB were assessed by western blot after treatment with formaldehyde at 0. 004,0. 02,0. 1 mmol/L. Results Compared with the control group,0. 5 ~ 12. 5 mmol/L formaldehyde exposure of formaldehyde 24 and 48 h could significantly reduce the viability of HepG2 cells( P〈0. 05). Caspase-3 expression levels were significantly decreased after 24 h exposure,and p53、p-p53( Ser15) 、mdm2 and RIP3 expression levels were decreased after both 24 and 48 h exposure.Only cleaved RIP1 expression levels were significantly increased after 24 and 48 h exposure. NF-κB expression levels were not significantly changed after 24 and 48 h exposure. Conclusion Formaldehyde exposure may induce apoptosis of HepG2 cells by death receptor pathway rather than mitochondrial pathway.
关 键 词:甲醛 HEPG2细胞 凋亡 受体相互作用蛋白激酶1
分 类 号:R114[医药卫生—卫生毒理学]
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