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Acute inflammation is accompanied by complement system activation and inflammatory cell accumulation. Acute kidney injury (AKI) is one of the common clinical symptoms, it is not clear whether complement system-mediated signaling pathway is involved. This study demonstrated that the expressions of complement C5a and C5a receptor (C5aR) protein in a mouse model with glycerol induced AKI were significantly increased, and the expression of inflammatory cytokines, such as IL-1β, IL-6 and TNF-α, were significantly higher than those in the blank control group. While C5aR antagonist (C5aRa) was added, western analyses for C5a and C5aR were reduced, meanwhile, qPCR and ELISA data showed that inflammatory cytokines also decreased significantly. In addition, preliminarily explored, the Mitogen-activated protein kinases (MAPKs) can be activated by the C5a/C5aR pathway in an AKI mouse model which showed that the C5a/C5aR pathway in a mouse model group activated ERK1/2 and p38, and the protein expression decreased when C5aRa was added. In conclusion, these results indicate that the C5a/C5aR pathway promotes renal pathogenesis by activating ERK1/2 and p38 expression and then affects the disease process, which has certain guiding significance for the subsequent clinical trial.

Association of C5a/C5aR pathway to activate ERK1/2 and p38 MAPK in acute kidney injury – a mouse model