Figure 1.

Lipid‐mediated oxidative stress, inflammation and impaired mitochondrial biogenesis can be rectified upon saroglitazar treatment. Results of cell viability in HepG2 cells treated with PA (0.75 mM) and various treatments for 16 h followed by MTT assay (A). The effect on mRNA levels of genes related to inflammation, mitochondrial biogenesis and antioxidants were measured using qPCR (B1, B2, B3). The cells were seeded into 60 mm dishes for flow cytometric analysis using the DCFDA dye specific for ROS generation (C). Immunoblotting was performed using phosphorylated and total NFkB and densitometric analysis was performed using ImageJ software (D). HepG2 cells were treated with PA (0.75 mM) and various treatments followed by measurement of oxygen consumption rate under basal respiratory conditions (E). The data were further used to calculate ATP production rate (F). Data are mean ±  SEM. ^# P < .05 and ^## P < .001 in comparison to control, *P < .05 and **P < .001 were considered significant in comparison to PA‐group. CAT, catalase; GPX, glutathione peroxidase; IL, Interleukin; MFN‐2, Mitofusin‐2; NFKB, nuclear factor kappa‐light‐chain‐enhancer of activated B cells; NRF‐1, Nuclear respiratory factor 1; OPA, optic atrophy; SOD1, superoxide dismutase 1; TNFα, tumour necrosis factor α