High Glucose Promotes CD36 Expression by Upregulating Peroxisome Proliferator-Activated Receptor γ Levels to Exacerbate Lipid Deposition in Renal Tubular Cells

Figure 4

The roles of AKT-PPARγ signaling pathway and CD36 in regulating HG-induced lipid accumulation in HK-2 cells. The HK-2 cells were transfected with CD36siRNA or nontargeting control siRNA (NTC siRNA) under HG (30 uM) and NG (5.6 uM) conditions and western blot analysis was used to determine CD36siRNA-mediated knockdown of CD36 in the HK-2 cells. Band intensities were normalized to β-actin band intensity using densitometry. The data from three independent experiments were represented as means ± SD (a). versus NTCsiRNA. By using Oil Red O staining, lipid content was detected in the HK-2 cells incubated with NG (5.6 mM), NG + NTCsiRNA, NG + CD36siRNA, NG + LY294002 (15 uM), NG + RSG (5 uM), NG + GW9662 (2.5 uM), HG (30 mM), HG + NTCsiRNA, HG + CD36siRNA, HG + LY294002 (15 uM), HG + RSG (5 uM), and HG + GW9662 (2.5 uM) for 48 h, respectively (b). Relative levels of lipid content were quantified by measuring relative absorbance of the eluted Oil Red O dye at 500 nm. Data from three independent experiments were represented as means ± SD (c). versus NG; versus HG.

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