Protective effects of antioxidants on chronic intermittent hypoxia-induced cardiac remodeling in mice
10.3760/cma.j.issn.0253-3758.2014.11.014
- VernacularTitle:抗氧化剂对慢性间歇性乏氧所致小鼠心肌重构的保护作用
- Author:
Xia YIN
1
;
Baicheng LI
;
Yuguang ZHAO
;
Weixia SUN
;
Yang ZHENG
Author Information
1. 吉林大学第一医院心血管疾病诊疗中心
- Keywords:
Sleep apnea,obstructive;
Ventricular remodeling;
Antioxidants;
Anoxia
- From:
Chinese Journal of Cardiology
2014;42(11):944-950
- CountryChina
- Language:Chinese
-
Abstract:
Objective Chronic intermittent hypoxia (CIH)animal model was used to mimic the status of obstructive sleep apnea (OSA) in order to investigate the pathological mechanism of CIH-induced cardiac remodeling and observe the protective effect of antioxidants.Methods FVB mice (8-10 weeksold) were randomly divided into control (saline,i.p.) group and CIH group,reduced form of nicotinamide adenine dinucleotide phosphate oxidase inhibitor,apocynin (APO,3 mg · kg-1 · d-1,i.p.) alone or CIH+APO,SOD mimic MnTMPyP (SODM,5 mg · kg-1 d-1,i.p.) alone or CIH + SODM (n =5 each).After 4 weeks,cardiac function and structure were determined by echocardiography,cardiac inflammation,apoptosis,cardiac fibrosis and cardiac MDA contents were examined by Western blot and chemical-biological methods,respectively.Results (1) Heart weight,LVIDd and LVIDs were increased while LYEF and FS were reduced in CIH group compared to control group (all P ＜ 0.05).(2) Myocardial protein expression of ANP and VCAM-1 was significantly upregulated,myocardial MDA content and apoptosis as well as myocardial fibrosis marker CTGF and PAI-1 were increased in CIH group compared to control group (all P ＜ 0.05).(3) Above parameters were similar between APO and CIH + APO as well as SODM and CIH + SODM (all P ＞ 0.05).Conclusion CIH could induce cardiac remodeling and CIH-induced cardiac inflammation,cardiac oxidative injury,cardiac apoptosis and cardiac fibrosis serve as the pathological mechanisms of CIH-induced cardiac remodeling.The protective effects of the two antioxidants suggest that the main mechanism of CIH-induced cardiac injury is oxidative stress.
