Cathelicidin-related antimicrobial peptide protects against ischaemia reperfusion-induced acute kidney injury in mice.

摘要: Background and purpose Despite recent advances in understanding its pathophysiology, treatment of acute kidney injury (AKI) remains a major unmet medical need, novel therapeutic strategies are needed. Cathelicidin-related antimicrobial peptide (CRAMP) with immunomodulatory properties has an emerging role various disease contexts. Here, we aimed to investigate the CRAMP underlying mechanisms AKI. Experimental approach The human homologue LL-37 were measured blood samples AKI patients experimental mice respectively. was induced wild-type CRAMP-deficient (Cnlp-/- ) by ischaemia/reperfusion (I/R). Therapeutic evaluation performed exogenous (5 mg·kg-1 , i.p.) treatment. Key results Cathelicidin expression inversely related clinical signs down-regulated renal I/R-induced mice. Cnlp-/- exhibited exacerbated dysfunction, aggravated inflammatory responses apoptosis. Moreover, over-activation NLRP3 inflammasome associated injury. Exogenous markedly attenuated response apoptosis, correlated modulation immune cell infiltration phenotype. Consistent mouse data, administration suppressed activation, protective effects mimicked specific inhibitor CY-09. reno-protective inhibitory required EGF receptor. Conclusion implications Our suggest that acts as mediator may represent potential strategy.