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ORIGINAL ARTICLE
Year : 2022  |  Volume : 65  |  Issue : 2  |  Page : 53-63

Adenosine mono-phosphate-activated protein kinase-mammalian target of rapamycin signaling participates in the protective effect of chronic intermittent hypobaric hypoxia on vascular endothelium of metabolic syndrome rats


1 Department of Physiology, Hebei Medical University; Department of Electron Microscopy Laboratory Centre, Hebei Medical University, Shijiazhuang, China
2 Department of Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China
3 Department of Physiology, Hebei Medical University, Shijiazhuang, China
4 Department of Electron Microscopy Laboratory Centre, Hebei Medical University, Shijiazhuang, China
5 Hebei Collaborative Innovation Center for Cardio-cerebrovascular Disease, Shijiazhuang, China
6 Department of Physiology, Hebei Medical University; Hebei Collaborative Innovation Center for Cardio-cerebrovascular Disease, Shijiazhuang, China

Correspondence Address:
Yi Zhang
Department of Physiology, Hebei Medical University, Shijiazhuang 050017
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cjp.cjp_84_21

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Our previous study demonstrated that chronic intermittent hypobaric hypoxia (CIHH) protects vascular endothelium function through ameliorating autophagy in mesenteric arteries of metabolic syndrome (MS) rats. This study aimed to investigate the role of adenosine mono-phosphate-activated protein kinase-mammalian target of rapamycin (AMPK-mTOR) signaling in CIHH effect. Six-week-old male Sprague-Dawley rats were divided into control (CON), MS model, CIHH treatment (CIHH), and MS + CIHH groups. Serum pro-inflammatory cytokines were measured. The endothelium dependent relaxation (EDR), endothelial ultrastructure and autophagosomes were observed in mesenteric arteries. The expression of phosphor (p)-AMPKα, p-mTOR, autophagy-related and endoplasmic reticulum stress-related proteins, p-endothelial nitric oxide synthase, and cathepsin D were assayed. In MS rats, pro-inflammatory cytokines were increased, EDR was attenuated, and endothelial integrity was impaired. In addition, the expression level of p-AMPKα and cathepsin D was down-regulated, but the level of p-mTOR was up-regulated. While in MS + CIHH rats, all aforementioned abnormalities were ameliorated, and the beneficial effect of CIHH was cancelled by AMPKα inhibitor. In conclusion, AMPK-mTOR signaling pathway participates in the protection of CIHH on vascular endothelium of MS rats.


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