Journal
SLEEP AND BREATHING
Volume 23, Issue 1, Pages 341-348Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s11325-018-1720-9
Keywords
Telmisartan; Intermittent hypoxia; Renal; Apoptosis; Autophagy
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Funding
- Xiamen Science and Technology Bureau [3502Z20154019]
- Fujian Provincial Health Bureau [2018-2-65]
- Natural Science Foundation of Fujian Province, China [2018J01393]
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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 12weeks. 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.
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