AIM:To investigate the role and mechanism of cell death-inducing DNA fragmentation factor al-pha(DFFA)-like effector B(Cideb)in promoting palmitic acid(PA)-induced lipid deposition in human hepatoblastoma HepG2 cells.METHODS:The HepG2 cells were divided into control group,model group,negative control silencing(siR-NC)group and Cideb silencing(siR-Cideb)group.The cells were treated with PA to establish a cellular model of lipid deposition.Specific siRNAs were used to silence the expression of Cideb,and the intracellular lipid content was mea-sured.Lipid deposition was observed by oil red O staining.RT-qPCR and Western blot were used to detect the expression levels of Cideb,sterol regulatory element-binding protein 1c(SREBP1c),acetyl-CoA carboxylase 1(ACC1),fatty acid synthase(FAS),stearoyl-CoA desaturase 1(SCD1)and AMP-activated protein kinase α(AMPKα)in the cells.The ef-fects of Cideb overexpression on HepG2 cells were observed by transfection with a Cideb eukaryotic expression plasmid.RESULTS:Compared with control group,the cells in PA model group presented lipid deposition,significantly increased triglyceride(TG)and total cholesterol(TC)content,elevated expression levels of Cideb,SREBP1c,ACC,FAS and SCD1,and decreased expression of AMPKα(P＜0.05).Compared with siR-NC group,the cells in siR-Cideb group pre-sented decreased lipid deposition,reduced intracellular TG and TC content,decreased SREBP1c,ACC,FAS and SCD1 expression levels,and increased AMPKα expression(P＜0.05).The overexpression of Cideb increased the lipid deposi-tion,TG and TC content,and the expression levels of SREBP1c,ACC,FAS and SCD1 in HepG2 cells,but decreased the expression of AMPKα(P＜0.05).CONCLUSION:Reduction of Cideb alleviates PA-induced lipid deposition in HepG2 cells by down-regulating the SREBP1c/ACC/FAS/SCD1 pathway and up-regulating the AMPKα pathway.

AIM:To investigate the role and mechanism of cell death-inducing DNA fragmentation factor al-pha(DFFA)-like effector B(Cideb)in promoting palmitic acid(PA)-induced lipid deposition in human hepatoblastoma HepG2 cells.METHODS:The HepG2 cells were divided into control group,model group,negative control silencing(siR-NC)group and Cideb silencing(siR-Cideb)group.The cells were treated with PA to establish a cellular model of lipid deposition.Specific siRNAs were used to silence the expression of Cideb,and the intracellular lipid content was mea-sured.Lipid deposition was observed by oil red O staining.RT-qPCR and Western blot were used to detect the expression levels of Cideb,sterol regulatory element-binding protein 1c(SREBP1c),acetyl-CoA carboxylase 1(ACC1),fatty acid synthase(FAS),stearoyl-CoA desaturase 1(SCD1)and AMP-activated protein kinase α(AMPKα)in the cells.The ef-fects of Cideb overexpression on HepG2 cells were observed by transfection with a Cideb eukaryotic expression plasmid.RESULTS:Compared with control group,the cells in PA model group presented lipid deposition,significantly increased triglyceride(TG)and total cholesterol(TC)content,elevated expression levels of Cideb,SREBP1c,ACC,FAS and SCD1,and decreased expression of AMPKα(P＜0.05).Compared with siR-NC group,the cells in siR-Cideb group pre-sented decreased lipid deposition,reduced intracellular TG and TC content,decreased SREBP1c,ACC,FAS and SCD1 expression levels,and increased AMPKα expression(P＜0.05).The overexpression of Cideb increased the lipid deposi-tion,TG and TC content,and the expression levels of SREBP1c,ACC,FAS and SCD1 in HepG2 cells,but decreased the expression of AMPKα(P＜0.05).CONCLUSION:Reduction of Cideb alleviates PA-induced lipid deposition in HepG2 cells by down-regulating the SREBP1c/ACC/FAS/SCD1 pathway and up-regulating the AMPKα pathway.

Objective To understand the activity concentrations of natural radionuclides ⁴⁰K, ²²⁶Ra, ²³²Th, and ²³⁸U in raw coal of coal mines in some regions of China, and to explore the correlation between ore with different activity concentrations and the concentration of radon and its progeny in the workplace. Methods Raw coal samples were collected in twelve coal mines in five provinces, and the activity concentrations of ⁴⁰K, ²²⁶Ra, ²³²Th, and ²³⁸U were measured by a high-purity germanium γ-ray spectrometric system. Results The activity concentrations of four natural radionuclides in the raw coal samples of twelve coal mines were all lower than 1000 Bq/kg, and the activity concentration of ²³⁸U in one coal mine was close to 100 Bq/kg. The content of ⁴⁰K, ²²⁶Ra, ²³²Th, and ²³⁸U in different coal mines varied greatly, but ²²⁶Ra, ²³²Th, and ²³⁸U were basically at the same level in the same coal mine. Conclusion None of the 12 coal mines belong to radio active mines. One of the coal mines investigated has the activity concentrations of ²²⁶Ra, ²³²Th, and ²³⁸U close to the standard limit for restricted-use management mines. It is suggested to study the correlation between the content of ²²⁶Ra in raw ore, intermediate products, tailings(slag), or other residues and the concentration of radon and its progeny in mines. Monitoring and protection of radon and its progeny in the decay chain should be strengthened for coal mines with high activity concentrations of natural radionuclides ²²⁶Ra, ²³²Th, and ²³⁸U.