Therefore, SLE could alleviate fibrosis development by its direct antioxidant effect and limit utilization of anti-oxidative enzymes, this restricts mitochondria over-oxidation of acetyl-CoA, as seen with the lower expression of Ppar-α and Cpt1a, and thus protect against fibrogenesis in WDS2 group, as shown with less Tgf-β1, Col1a1 and Timp1 mRNA. This evidence concerns the gene PPARA and systemic lupus erythematosus.