The proximal tubular α7 nicotinic acetylcholine receptor attenuates ischemic acute kidney injury through Akt/PKC signaling-mediated HO-1 induction.

ABSTRACT: Activation of the α7 nicotinic acetylcholine receptor (α7nAChR) has been shown to attenuate excessive inflammation by inhibiting proinflammatory cytokines during ischemia-reperfusion (IR) injury; however, the underlying kidney-specific molecular mechanisms remain unclear. The protective action of α7nAChR against renal IR injury was investigated using a selective α7nAChR agonist and antagonist. α7nAChR activation reduced plasma creatinine levels and tubular cell damage, whereas α7nAChR inhibition aggravated the IR-induced phenotype. α7nAChR activation decreased neutrophil infiltration and proinflammatory cytokine expression, increased heme oxygenase-1 (HO-1) expression, and reduced proximal tubular apoptosis after IR as shown by terminal deoxynucleotidyl transferase dUTP nick-end labeling s

SUBMITTER: Kim H 

PROVIDER: S-EPMC5938048 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature