张林伟, 薛璟, 肖杭, 高蓉, 王军. 双酚F引起的脂质降解能力降低引发非酒精性脂肪性肝病脂质积聚的作用研究[J]. 职业卫生与应急救援, 2023, 41(2): 215-219. DOI: 10.16369/j.oher.issn.1007-1326.2023.02.020
引用本文: 张林伟, 薛璟, 肖杭, 高蓉, 王军. 双酚F引起的脂质降解能力降低引发非酒精性脂肪性肝病脂质积聚的作用研究[J]. 职业卫生与应急救援, 2023, 41(2): 215-219. DOI: 10.16369/j.oher.issn.1007-1326.2023.02.020
shu
ZHANG Linwei, XUE Jing, XIAO Hang, GAO Rong, WANG Jun. In vitro study on the role of reduced lipid degradation capacity induced by bisphenol F in triggering lipid accumulation in nonalcoholic fatty liver disease[J]. Occupational Health and Emergency Rescue, 2023, 41(2): 215-219. DOI: 10.16369/j.oher.issn.1007-1326.2023.02.020
Citation: ZHANG Linwei, XUE Jing, XIAO Hang, GAO Rong, WANG Jun. In vitro study on the role of reduced lipid degradation capacity induced by bisphenol F in triggering lipid accumulation in nonalcoholic fatty liver disease[J]. Occupational Health and Emergency Rescue, 2023, 41(2): 215-219. DOI: 10.16369/j.oher.issn.1007-1326.2023.02.020
shu

双酚F引起的脂质降解能力降低引发非酒精性脂肪性肝病脂质积聚的作用研究

In vitro study on the role of reduced lipid degradation capacity induced by bisphenol F in triggering lipid accumulation in nonalcoholic fatty liver disease

    摘要
  • 摘要:
      目的  从脂质降解角度，阐述双酚F（bisphenol F，BPF）暴露对肝脏细胞HepG2脂质降解能力、脂肪酸氧化、活性氧（reactive oxygen species，ROS）水平三方面的影响。
      方法  采用HepG2构建体外染毒模型，通过实时聚合酶链式反应（polymerase chain reaction，PCR）、共聚焦显微镜检测及Western blot等实验技术，观察BPF对HepG2细胞的脂质降解途径的影响。
      结果  BPF暴露引起HepG2细胞脂质水解限速酶——脂肪三酰甘油脂肪酶及激素敏感性脂肪酶mRNA及蛋白表达减少（P < 0.05）；脂肪酸氧化相关蛋白——肉碱棕榈酰转移酶1α（CPT1α）、过氧化物酶体增殖物激活受体α（PPARα）mRNA及蛋白表达降低（P < 0.05），线粒体来源的ROS水平升高（P < 0.01）；最终导致脂滴积聚。
      结论  BPF暴露致HepG2细胞脂质降解和脂肪酸氧化能力降低，以及线粒体来源ROS水平升高，可能是造成非酒精性脂肪性肝病样改变发生的重要原因之一。

     

    Abstract:
      Objective  From the perspective of lipid degradation, the effects of bisphenol F (BPF) exposure on lipolysis, fatty acid oxidation, and reactive oxygen species (ROS) levels in HepG2 cells were described.
      Methods  HepG2 cells were used to construct an in vitro exposure model. The effects of BPF on the lipid degradation pathway were observed by real-time quantitative PCR, confocal microscopy, and Western blot.
      Results  BPF exposure reduced the mRNA and protein expression of the rate-limiting enzymes, adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in HepG2 cells (P < 0.05). The mRNA and protein expressions of the fatty acid oxidation-related proteins, carnitine palmitoyl transferase 1α (CPT1α) and peroxisome proliferator-activated receptor α (PPAR α), were decreased (P < 0.05), and the ROS level from mitochondria was increased (P < 0.01). This caused the accumulation of lipid droplets.
      Conclusions  BPF exposure reduced lipolysis and fatty acid oxidation in HepG2 cells and increased the level of ROS derived from mitochondria, which may be one of the important reasons for the occurrence of nonalcoholic fatty liver disease (NAFLD)-like changes.

     

    • HTML全文
    • 参考文献(33)
    • 相关文章
    • 施引文献
  • 资源附件(0)

/

返回文章
返回