甲醛对HepG2细胞脂肪代谢的影响

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-binding protern-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 comlex Ⅰ，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。

Effects of formaldehyde on lipid metabolism in HepG2 cells

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.