Treatment of diabetic mice with GLP-1 receptor agonists inhibits NAD(P)H oxidase activity, reducing renal oxidative stress [21], and promotes the resolution of inflammation via attenuating production of bone marrow-derived progenitor cells and kidney inflammation [22] and thus RS may limit renal oxidative stress, inflammation, and subsequent kidney injury via a GLP-1-mediated mechanism. This evidence concerns the gene GLP1R and medical procedure.