山茶油对游离脂肪酸诱导的HepG2细胞脂质代谢的影响

目的:探究山茶油对游离脂肪酸诱导的HepG2细胞脂质代谢的影响。方法:首先,利用CCK8法测定不同浓度山茶油对HepG2细胞活性的影响以选定适宜浓度进行后续实验。其次,采用不同浓度山茶油对HepG2细胞进行24 h干预,再使用0.5 mmol/L游离脂肪酸处理24 h诱导建立脂肪肝细胞模型。然后,通过油红O染色法判断各组间的脂滴生成情况,并参照相关试剂盒测定各干预下细胞内脂质水平的变化情况。最后,通过qRT-PCR法测定细胞内脂质代谢相关基因的表达,以探讨山茶油调节脂质代谢的作用及其可能的机制。结果:与正常对照组相比,造模干预组细胞内的甘油三酯(TG)和低密度脂蛋白胆固醇(LDL-C)含量显著升高(P<0.05),高密度脂蛋白胆固醇(HDL-C)含量显著降低(P<0.05);与造模干预组相比,茶油预处理显著逆转了游离脂肪酸诱导细胞内TG、HDL-C和LDL-C含量的变化(P<0.05)。qRT-PCR结果表明,与造模干预组相比,山茶油预处理显著降低了游离脂肪酸诱导的HepG2细胞内脂肪酸转运酶(CD36)、固醇调节元件结合蛋白-1c(SREBP-1c)、脂肪酸合成酶(...

Effect of Camellia Oil on Lipid Metabolism of HepG2 Cells Induced by Free Fatty Acids

Objective: To evaluate the effects of camellia oil on lipid metabolism in free fatty acid-induced HepG2 hepatocytes. Methods: To screen the optimal concentration of action, the effect of camellia oil on HepG2 activity was assessed by CCK-8 assay. HepG2 cells were exposed to different concentrations of camellia oil for 24 h, after which the cells were treated with 0.5 mmol/L free fatty acids for 24 h to induce in vitro model of liver steatosis. Then, intracellular lipid content was detected using Oil Red O staining. Lipid profiles were measured by commercial kits. The mRNA expression of genes related to lipid metabolism was measured by qRT-PCR to investigate the effects and possible mechanisms of camellia oil in regulating lipid metabolism. Results: Compared with the normal control group, fatty acids induction significantly increased the contents of triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) (P<0.05), and decreased the content of high-density lipoprotein cholesterol (HDL-C) (P<0.05). Interestingly, camellia oil pretreatment significantly reversed the changes in intracellular contents of TG, HDL-C and LDL-C induced by fatty acids incubation (P<0.05). In addition, compared with the model group, camellia oil pretreatment significantly decreased the mRNA expression of fatty acid transporter (CD36), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), sterol regulatory element-binding protein-1c (SREBP-1c), and peroxisome proliferator-activated receptor γ (PPARγ) (P<0.05), and increased the mRNA expression of adipose triglyceride lipase (ATGL), peroxisome proliferator-activated receptor alpha (PPARɑ), and carnitine palmitoyltransferase-1A (CPT1A) (P<0.05). Conclusions: Camellia oil may alleviate the lipid metabolism disorder induced by free fatty acids in HepG2 cells partly by modulating the expression levels of genes involved in lipid lipogenesis and oxidation.