Danlou tablet ameliorates lipid deposition in HepG2 cells by regulating oxidative stress
10.12007/j.issn.0258-4646.2025.10.001
- VernacularTitle:丹蒌片通过调控氧化应激改善HepG2细胞脂质沉积
- Author:
Zhiqi SONG
1
;
Nan SONG
;
Yu LIU
;
Jingnan LIU
;
Qun WANG
;
Lianqun JIA
;
Dongyu MIN
Author Information
1. 辽宁中医药大学 第一临床学院,沈阳 110847
- Publication Type:Journal Article
- Keywords:
Danlou tablet;
lipid deposition;
oxidative stress;
HepG2 cell
- From:
Journal of China Medical University
2025;54(10):865-868,882
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate whether Danlou tablet-containing serum ameliorates lipid deposition in HepG2 cells by regulating oxidative stress.Methods Optimal treatment conditions,including concentration and exposure time of Danlou tablet and concentration of oleic acid,were determined,and their effects on cell viability were assessed using the CCK-8 assay.An in vitro model of lipid depo-sition was established by inducing HepG2 cells with oleic acid.HepG2 cells were divided into control,model(treated with oleic acid),and Danlou tablet groups(treated with oleic acid and Danlou tablet).Intracellular lipid droplets were visualized using oil red O staining.Lipid content including non-esterified fatty acid(NEFA)and triglyceride(TG),as well as oxidative stress markers in the cell supernatant,were quantified by enzyme-linked immunosorbent assay.Ultimately,reactive oxygen species(ROS)levels were measured using a fluores-cent probe.Results The optimal conditions were 10%Danlou tablet,24-hour treatment,and 800 μmol/L oleic acid.Compared with the control group,the model group exhibited significantly increased lipid droplet number and size,elevated supernatant levels of NEFA,TG,malondialdehyde,cyclooxygenase-2,and ROS(P<0.01),and decreased levels of catalase and superoxide dismutase(P<0.01).Compared with the model group,the Danlou tablet group showed reduced lipid deposition and oxidative stress markers,and increased antioxidant enzyme activity.Conclusion Danlou tablet may ameliorate oleic acid-induced lipid deposition in HepG2 cells by regulating oxidative stress response.