Abstract
PurposeObstructive sleep apnea (OSA) is associated with renal impairs. As a novel pathophysiological hallmark of OSA, chronic intermittent hypoxia (CIH) enhances apoptosis and autophagy. The present study aims to evaluate the effect of telmisartan on CIH-induced kidney apoptosis and autophagy in a mouse model of OSA.Materials and methodsMice were randomly allocated to normoxia, CIH, and CIH+telmisartan groups (n = 12 in each group). The CIH exposure duration was 12 weeks. Mice in the CIH+telmisartan group received telmisartan administration. The terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and western blotting of Bax and cleaved caspase-3 were conducted for evaluating apoptosis in kidney tissue. While the autophagy-related proteins, beclin-1 and LC3, were also observed via western blotting.ResultsThe percentage of apoptotic cell in the CIH group was significantly higher than that of normoxia group; meanwhile, Bax and cleaved caspase-3 protein levels were increased in the CIH group than those of normoxia group (all p < 0.05). Compared with the normoxia group, mice in the CIH group had greater autophagy-related proteins (beclin-1 and LC3) expression. When compared to the CIH group, both the renal apoptosis and autophagy in the CIH+telmisartan group were decreased.ConclusionThe CIH accelerates renal apoptosis and autophagy levels. Telmisartan ameliorating those levels suggests that it might prevent renal impairs from the CIH in OSA patients.
Highlights
Obstructive sleep apnea (OSA) is a highly prevalent medical disorder among middle-age adults [1]
The percentage of apoptotic cell in the chronic intermittent hypoxia (CIH) group was significantly higher than that of normoxia group; Bax and cleaved caspase-3 protein levels were increased in the CIH group than those of normoxia group
The present study aims to evaluate the effect of CIH on renal apoptosis and autophagy and further to assess the influence of telmisartan on those in a mouse model
Summary
Obstructive sleep apnea (OSA) is a highly prevalent medical disorder among middle-age adults [1]. Accumulated data confirmed the bidirectional association between kidney diseases and OSA; for one thing, the incidence and mortality of OSA in kidney disease are higher than those in general population; for the other, OSA contributes the impairs of renal function [2, 3]. Our previous studies indicated that cystatin C, a biomarker of early renal impairs, was higher in several OSA patients without complications [4], and continuous positive airway pressure (CPAP) treatment can normalize cystatin C levels in those. The potential mechanisms of OSA-related renal impair are inconclusive. Previous studies elucidated that OSA leads to renal impairs thorough hypertension, sympathetic nervous system and renin-angiotensin-aldosterone system overactivation, endothelial dysfunction, and increased oxidative stress [6, 7]
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