Inflammation plays a central mechanism in the initiation and maintenance of kidney injury, and a suppressed inflammatory response reduces the extent of renal fibrosis.43, 44 Our results indicate that administering petA to prevent or treat UUO can suppress the expression of multiple proinflammatory cytokines, such as TNF‐α, IL‐β, MCP‐1 and IL‐6, and inhibit macrophage infiltration, suggesting that inhibition of the inflammatory response is also one of the mechanisms by which petA ameliorates renal fibrosis. Here, CCL2 is linked to renal fibrosis.