Artemisinin Research Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Molecules. 2022 Mar 18;27(6):1978. doi: 10.3390/molecules27061978.
Garcinia biflavonoid 1 (GB1) is one of the active chemical components of and is reported to be capable of reducing the intracellular lipid deposition, which is the most significant characteristic of non-alcoholic fatty liver disease. However, its bioactive mechanism remains elusive. In the current study, the lipid deposition was induced in HepG2 cells by exposure to oleic acid and palmitic acid (OA&PA), then the effect of GB1 on lipid metabolism and oxidative stress and the role of regulating PPARα in these cells was investigated. We found that GB1 could ameliorate the lipid deposition by reducing triglycerides (TGs) and upregulate the expression of PPARα and SIRT6, suppressing the cell apoptosis by reducing the oxidative stress and the inflammatory factors of ROS, IL10, and TNFα. The mechanism study showed that GB1 had bioactivity in a PPARα-dependent manner based on its failing to improve the lipid deposition and oxidative stress in PPARα-deficient cells. The result revealed that GB1 had significant bioactivity on improving the lipid metabolism, and its potential primary action mechanism suggested that GB1 could be a potential candidate for management of non-alcoholic fatty liver disease.
藤黄双黄酮 1（GB1）是藤黄属植物的一种活性化学成分，据报道，它能够减少细胞内脂质沉积，这是非酒精性脂肪肝疾病的最显著特征。然而，其生物活性机制尚不清楚。在本研究中，通过用油酸和棕榈酸（OA&PA）孵育 HepG2 细胞来诱导脂质沉积，然后研究了 GB1 对脂质代谢和氧化应激的影响以及其在这些细胞中调节过氧化物酶体增殖物激活受体α（PPARα）的作用。我们发现，GB1 可以通过降低三酰甘油（TGs）来改善脂质沉积，并上调 PPARα 和 SIRT6 的表达，通过降低氧化应激和活性氧（ROS）、白细胞介素 10（IL10）和肿瘤坏死因子-α（TNFα）等炎症因子来抑制细胞凋亡。机制研究表明，GB1 具有 PPARα 依赖性的生物活性，因为它不能改善 PPARα 缺陷细胞中的脂质沉积和氧化应激。结果表明，GB1 对改善脂质代谢具有显著的生物活性，其潜在的主要作用机制表明，GB1 可能是治疗非酒精性脂肪性肝病的潜在候选药物。
