Objective To investigate the regulatory effect of inhibiting peroxisome proliferator-activated receptor gamma (PPARγ) on CD36 expression and lipid accumulation during the foaming of alveolar macrophages induced by free silica (SiO2).
Methods Rat alveolar macrophage strain NR8383 cells were cultured in vitro. The PPARγ pathway was blocked by inhibitor GW9662. The foaming of the cells was observed. The cells were divided into inhibitor (GW9662), solvent control (DMSO), experiment (GW9662+SiO2+ox-LDL), and model (DMSO+SiO2+ox-LDL) groups, and cultured for 36 h. Oil red O staining was used to observe the accumulation of lipid. The expressions of intracellular total cholesterol and free cholesterol were detected by enzyme assay to calculate the ratio of cholesterol ester to total cholesterol and identify the formation of foam cells. Western blot and real-time fluorescence PCR were used to detect the protein and gene expressions of PPARγ and CD36.
Results The total cholesterol levels in the experiment group(8.78±0.49) mg/g, inhibitor group(6.23±0.27) mg/g, and solvent control group(6.99±0.30) mg/g were significantly lower than that in the model group(31.41±1.36) mg/g (P < 0.05). The cholesterol ester/total cholesterol ratio was less than 50% in the experiment group (28.43%), inhibitor group (27.02%), and solvent control group (24.92%), and there was no difference among the three groups (P > 0.05). The number of foam cells in the experiment group was significantly reduced compared with the model group. Both the CD36 protein (0.55±0.13) and mRNA (1.30±0.39) expression levels of the inhibitor group were significantly lower than those of the model group(1.08±0.31), (3.38±0.70) (P < 0.05).
Conclusion CD36 expression induced by free SiO2 may be mediated by PPARγ.
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