RESUMEN
Objective To investigate the molecular mechanism of palmitic acid (PA) inducing inflammation and epithelial to mesenchymal transdifferentiation (EMT) in human renal tubular epithelial cells (RTECs). Methods The cell lipid accumulation model was prepared by RTECs and the cells were divided into blank control group, bovine serum albumin (BSA) group, PA group, and PA combined with stimulator of interferon genes (STING) specific inhibitor H151 group. The lipid accumulation of RTECs were detected by oil red O staining. Real-time quantitative PCR was used to detect the mRNA levels of interleukin 6 (IL-6), IL-8, transforming growth factor ß1 (TGF-ß1), and type 1 collagen alpha 1 chain (COL1A1) in RTECs. The protein expressions of STING, nuclear factor-κB p65 (NF-κB p65), phosphorylated NF-κB p65 (p-NF-κB p65), TGF-ß1, and type 1 collagen (Col1) were detected by Western blot and the expression and distribution of Col1 in RETCs were detected by immunofluorescence chemical staining. Results Compared with the control group, PA stimulated the lipid deposition, the expression of STING, and the phosphorylation of NF-κB p65 obviously, up-regulated the mRNA levels of IL-6, IL-8, TGF-ß1, and COL1A1 significantly, increased the protein expressions of TGF-ß1 and Col1 and the distribution of Col1 in RTECs; compared with those in the PA group, after H151 treatment, the expression of STING and the phosphorylation of NF-κB p65 decreased notably, the mRNA levels of IL-6, IL-8, TGF-ß1, and COL1A1 were down-regulated dramatically, and the protein expressions of TGF-ß1 and Col1 declined with reduced distribution of Col1. Conclusion PA induces lipid deposition, activated the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)/STING pathway, and caused inflammation and EMT in RTECs.