Abstract
ObjectiveIschemic injury is one of the major causes of acute kidney injury (AKI), and inflammation plays an important role in the ischemic AKI. M2 macrophages had shown antimicrobial and anti‐inflammatory activities, but its effect on AKI has not been reported. This study aims to improve the protection of peritoneal M2 macrophage on renal function in an ischemic AKI model.MethodsThe macrophages (M0) were isolated from peritoneal dialysate of normal mice, and then induced to M2 by IL‐4/IL‐13. Male C57/BL6 mice were randomly divided into three groups: Control, IRI, and IRI+M2. The IRI mice were made by clamping renal pedicles for 30 minutes. After reperfusion, IRI+M2 group mice were injected with M2 macrophage (1×106 cell dissolved in 50 μL PBS) into capsule of kidney. .All mice were scarified at 3 days after surgery, then, the serum creatinine (Scr), blood urea nitrogen (BUN) and uric acid (UA) were measured. Renal pathology was observed by HE and PAS staining. The renal population of M2 /M1 macrophage was analyzed by flow cytometry. Pro‐inflammatory cytokines (IL‐1β/IL‐6/TNF‐α/iNOS) gene expression in kidney of mice were analyzed by real‐time PCR (qPCR).ResultsAfter 3 days of surgery, IRI mice had increased levels of BUN, Scr and UA compared to control, whereas injected with M2 macrophage significantly reduced BUN, Scr and renal tubular injury score in IRI mice, and the M2/M1 ratio in kidney of IRI+M2 group was significantly higher than IRI mice. In addition, the mRNA levels of inflammatory cytokines (IL‐1β, IL‐6, TNF‐α, and iNOS) in the IRI+M2 mice were significantly lower than those in IRI mice.ConclusionThese results indicated that peritoneal M2 macrophages could effectively reduce inflammatory response and kidney injury in IRI mice, and thus it may serve as a potential cell therapy for renal diseases.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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