Affiliation:
1. Department of Gerontology, Cangzhou Central Hospital, No.16 Xinhua West Road, Cangzhou, Hebei 061000, China
Abstract
Background:
Ischemia-reperfusion (IR) injury is one of the major causes of acute kidney
injury (AKI). Chemerin chemokine-like receptor 1 (CMKLR1) has been reported to be involved in the
progression of IR injury. Here, we investigated the protective role of CMKLR1 antagonist, α-NETA, in
IR mouse model, and dissected the underlying regulatory mechanism.
Methods:
IR injury mouse model was established to evaluate the protective effects of α-NETA on IR
injury. Kidney injury-associated parameters and functions were examined to evaluate the renal function
of Sham, IR, and IR+ α-NETA mice. Renal morphological changes and apoptosis were determined by
PAS and TUNEL staining in IR and α-NETA treated mice. ELISA, RT-qPCR, and western blot were
performed to examine the inflammatory responses and expression of CMKLR1.
Results:
α-NETA administration attenuated IR-induced renal tubular injury and epithelial cell apoptosis
in IR injury mice. Kidney injury-related cystatin C, kidney injury molecule-1, neutrophil gelatinaseassociated
lipocalin, and renal morphology were significantly improved. Mechanistically, α-NETA
suppressed the inflammatory responses by inhibiting the expression of CMKLR1, and then protected
the IR-induced renal damage and restored renal function.
Conclusion:
CMKLR1 plays an important role in renal ischemia-reperfusion injury, targeting
CMKLR1 by using the small molecule inhibitor α-NETA is a potential treatment strategy for AKI.
Publisher
Bentham Science Publishers Ltd.
Subject
Biochemistry,General Medicine,Structural Biology
Cited by
1 articles.
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