Reports have demonstrated lower lipid peroxidation of n-3 fatty acids that modulate oxidative responses in subjects exposed to stress. This may be associated with the assembly of n-3 fatty acid into lipoproteins and the reduced opportunity for free radical attack of double bonds, inhibition of phospholipase A2 and stimulation of antioxidant enzymes. N-3 fatty acids were shown to act both by replacing eicosanoid substrate AA and inhibiting AA metabolism and by altering inflammatory gene expression through transcription factor activation. 5-HETE is a metabolite of AA metabolized by P450 enzymes. Interestingly, the level of 5-HETE was reversed closer to control level in the CKD + Ergone group. Addition of AA to mesangial cells could induce upregulation of TGF-b1, CTGF, fibronectin and collagen IV expression, while EPA and DHA had no stimulatory effects on mesangial cells. On the contrary, the co-exposure of cells to EPA and DHA could suppress the AA-induced upregulation of TGF-b1, fibronectin, CTGF and collagen IV expression, which were consistent with our protein expression results. Uremic toxins including IS and p-CS contributed to the pathological process of CKD. A previous study demonstrated a significant association between serum IS and p-CS levels and CKD progression. Accumulating evidence has demonstrated that IS and p-CS had important effects on chronic kidney injury. Increased renal IS and p-CS were observed in the CKD group PD325901 compared with control group and a beneficial decreased renal IS and p-CS were revealed in the CKD + Ergone group. TGF-b1 was recognized as both a fibrogenic and inflammatory cytokine and played a critical role in kidney injury. It was reported that IS could upregulate TGF-b1 expression in uremic kidney, which enhances the renal expression of tissue inhibitor of metalloproteinase-1 and collagen I, leading to CKD progression. Another study showed that decreased IS with uremic toxin binders could significantly downregulate TGF-b1 expression. The current results demonstrated that ergone could downregulate TGF-b1 and collagen I protein expression by promoting decreases of IS and p-CS in the CKD group. Amino acids were substrates for metabolic energy, protein synthesis, gluconeogenesis and ketogenesis. Increased renal phenylalanine and tryptophan were observed in the CKD + Ergone group compared with the CKD group. A major metabolic pathway of phenylalanine is its hydroxylation by phenylalanine hydroxylase to tyrosine. It was reported that decreased phenylalanine was observed in kidney medullar tissue, plasma and urine of adenineinduced CKD rats compared with control rats. Also consistent with this observation was the finding that phenylalanine was higher in CKD patients than in healthy subjects. A separate 1 H NMR metabonomics showed increased serum phenylalanine was observed in both low-risk immunoglobulin A nephropathy patients and high-risk patients with nephropathies. Tryptophan was either incorporated into proteins or broken down for energy and metabolic intermediates.