Objective: Elevated hepatocyte oxidative stress and inflammation may trigger lipid accumulation and promote the formation of NAFLD. As a new member of the ANGPTL family, ANGPTL7 plays an important role in inflammatory responses, angiogenesis and oxidative stress. However, whether ANGPTL7 participates in the pathogenesis of NAFLD still remains unknown. Therefore, in this study, we investigated the role of ANGPTL7 in HepG2 cells.
Methods: HepG2 cells were divided into control group (pcDNA3.1(+)), ANGPTL7 overexpression group (Angptl 7 OE ) and ANGPTL7 overexpression group with STAT3 knockdown group (Angptl 7 OE + si-STAT3). Cell viability was assessed by CCK-8 assay. Cell lipid level was checked by oil red O staining. Cellar IL-6, TNF-α, ROS, MDA, SOD and GSH level were determined by kits. The expression of ANGPTL7, STAT3, iNOS and COX-2 were measured by RT-PCR and western blot.
Results: Compared with CON group, ANGPTL7 overexpression led to elevated cellular IL-6, TNF-α, ROS and MDA, and reduced GSH and SOD, and increased expression of STAT3, iNOS and COX-2, indicating promoted oxidative stress and inflammatory responses. All these alterations caused by ANGPTL7 can be partly reversed by STAT3 knockdown.
Conclusion: Angptl7 could cause oxidative stress and inflammatory response partly via activating STAT3 in HepG2 cells.
Q. Gao: None. Y. Zhou: None. Y. Liu: None. M. Li: None. M. Gao: None.
