摘要
目的:探讨甲醛对HepG2细胞甘油三酯(triglyceride,TG)含量的影响及其可能机制。方法:以0.02、0.1、0.5、2.5、12.5 mmol/L的甲醛(formaldehyde,FA)分别处理人肝癌HepG2细胞24和48 h,采用CCK-8法检测细胞活性,GPO-POD酶法测定细胞内TG含量。另分别以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法检测肉碱棕榈酰转移酶1(carnitine palmitoyl transferase 1,CPT1)、固醇调节元件结合蛋白-1c(sterol regulatory element-bindingprotern-1c,SREBP-1c)、腺苷酸核糖基化因子1(ADP-ribosylation factor 1,Arf1)和包被蛋白Ⅰ(coat protein comlexⅠ,COPⅠ)的蛋白表达水平。结果:与对照组比较,0.5~12.5 mmol/L FA染毒24 h或0.1~12.5 mmol/L染毒48 h时可显著降低HepG2细胞活性(P均<0.05);0.1 mmol/L FA染毒24 h,或者0.1和0.02 mmol/L FA染毒48 h,均可致HepG2细胞内TG含量显著升高(P均<0.05);FA染毒48 h引起肝细胞内CPT1表达水平明显降低(P均<0.05),SREBP-1c和COPⅠ表达水平在染毒24和48 h后均增高(P均<0.05),FA染毒24 h后Arf1表达水平明显增加(P<0.05)。结论:FA接触可引起HepG2细胞内TG含量增加,其机制可能与脂肪酸β氧化受到抑制和脂肪合成增加有关。
OBJECTIVE: To investigate the effects and possible mechanism of liquid formaldehyde on the triglyceride content of HepG2 hepatocytes. METHODS: HepG2 ceils were treated with formaldehyde in 0.02, 0.1, 0.5, 2.5 and 12.5 mmol/L concentrations, CCK-8 method was used to detect cell viability. Triglyceride was measured by triglyceride GPO-POD assay kit after formaldehyde exposure. The expression of carnitine palmitoyl transferase 1 (CPT1), sterol regulatory element-binding protein(SREBP) lc, ADP-ribosylation factor 1 (Arfl) and coat protein comlex I (COP I ) were assessed by western blot after treatment with formaldehyde in 0.004, 0.02, 0.1 mmol/L concentrations. RESULTS: 0.5 - 12.5 mmol/L FA exposure of 24 h or 0.1-12.5 mmol/L FA exposure of 48 h could significantly reduce the viability of HepG2 cells (P〈0.05). TG contents were increased significantly after exposure to 0.1 mmol/L FA for 24 hours or 0.1 and 0.02 mmol/L FA for 48 h(P〈0.05). CPT1 expression levels were significantly decreased after 48 h exposure, but SREBP-lc and COP I expression levels were increased after both 24 h and 48 h exposures. Arfl expression level was significantly increased after 24 h exposure. CONCLUSION: FA exposure could increase intracellular TG contents in HepG2 cells, and it may be associated with inhibition of fatty acid [3 oxidation and increased synthesis of triglyceride.
出处
《癌变.畸变.突变》
CAS
CSCD
2013年第6期416-421,共6页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
山西省回国留学人员科研资助项目(2009-53)