Hepatic-specific vitamin D receptor downregulation alleviates aging-related metabolic dysfunction-associated steatotic liver disease

Figure 4 Downregulation of vitamin D receptor alleviated palmitic acid-induced steatosis when cellular senescence was induced. A: Protein expression level of the vitamin D receptor (VDR) and corresponding quantitative results, and mRNA level of VDR in AML12 cells transfected with the small interfering-negative control (siNC) or the VDR knockdown construct small interfering-VDR (siVDR); B: Protein expression level of VDR and corresponding quantitative results, and mRNA level of VDR in HepG2 cells treated with siNC or siVDR; C and D: Cellular levels of triglycerides and Oil Red O staining (× 400) of AML12 cells treated with hydrogen peroxide (H₂O₂) (400 μM) for 6 hours, transfected with siNC or siVDR, and stimulated with palmitic acid (PA) (300 μM) for 24 hours; E and F: Cellular levels of triglycerides and Oil Red O staining (× 400) of HepG2 cells treated with H₂O₂ (400 μM) for 6 hours, transfected with siNC or siVDR, and stimulated with PA (300 μM) for 24 hours. Protein levels and mRNA levels were normalized to those of glyceraldehyde-3-phosphate dehydrogenase. The data are presented as the means ± SDs. ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. P calculated as determined via student’s t tests and one-way analysis of variance with Tukey’s correction. VDR: Vitamin D receptor; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; si-NC: Small interfering-negative control; si-VDR: Small interfering-vitamin D receptor; H₂O₂: Hydrogen peroxide; BSA: Bovine serum albumin; PA: Palmitic acid.