Telmisartan attenuates kidney apoptosis and autophagy-related protein expression levels in an intermittent hypoxia mouse model

• DOI: 10.1007/s11325-018-1720-9
• Publication Date: 2018-09-16T08:14:23Z
• Authors: Xiao-Bin Zhang; Jing-Huang Cai; Yu-Yun Yang; Yi-Ming Zeng; Hui-Qing Zeng; Miao Wang; Xiao Cheng; Xiongbiao Luo; Henry Chidozie Ew...
• Keywords: Telmisartan; Terminal deoxynucleotidyl transferase; Hypoxia

Obstructive 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 telmisartan on CIH-induced kidney autophagy in mouse model OSA.Mice were randomly allocated normoxia, CIH, CIH+telmisartan groups (n = 12 each group). CIH exposure duration was weeks. Mice group received administration. terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay western blotting Bax cleaved caspase-3 conducted for evaluating tissue. While autophagy-related proteins, beclin-1 LC3, also observed via blotting.The percentage apoptotic cell significantly higher than that normoxia group; meanwhile, protein levels increased those (all p < 0.05). Compared group, mice had greater proteins (beclin-1 LC3) expression. When compared both decreased.The accelerates levels. Telmisartan ameliorating suggests it might prevent impairs from OSA patients.