Fig. 3

IKK inhibitor alleviated lipid deposition and oxidative stress injury in cells exposed to ox-LDL. HK-2 cells were exposed to ox-LDL to construct a cell model. TPCA1 acted as an IKK inhibitor. Cells were divided into three groups: control, ox-LDL, and ox-LDL + TPCA1. A TG levels of treated cells. B Representative Oil Red O staining of HK-2 cells in different groups. C and D qRT–PCR analysis of MAD levels and SOD activity in HK-2 cells in different groups. E DHE staining of intracellular ROS levels. F ΔΨm was measured using the JC-1 assay in treated HK-2 cells. IKK, IκB kinase; ox-LDL, oxidized low-density lipoprotein; HK-2, human kidney 2; TPCA-1, 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide; TG, triglyceride; qRT–PCR, real-time quantitative reverse transcription PCR; MAD, malondialdehyde; SOD, superoxide dismutase; DHE, dihydroethidium; ROS, reactive oxygen species; ΔΨm, mitochondrial membrane potential. Significance was assessed by an ANOVA test. The experimental data are shown as the mean ± SD. N = 3. *P < 0.05, **P < 0.01, ***P < 0.001