The effects of vitamin D deficiency on the cardiac oxidative stress in mice and the underlying mechanisms
10.16571/j.cnki.1008-8199.2016.10.009
- VernacularTitle:维生素D缺乏对小鼠心肌氧化应激水平的影响及机制研究
- Author:
Yi TANG
;
Jing LIU
;
Liang XIE
;
Lijun WANG
;
Qigao ZHANG
;
Yongping PENG
;
Jianbin GONG
;
Shisen JIANG
- Publication Type:Journal Article
- Keywords:
Vitamin D;
Oxidative stress;
Cardiac remodeling;
Aptosis
- From:
Journal of Medical Postgraduates
2016;29(10):1050-1054
- CountryChina
- Language:Chinese
-
Abstract:
Objective Previous studies have shown that vitamin D deficiency is closely related to cardiac remodeling. How?ever, the underlying mechanisms have not been fully elucidated. Moreover, oxidative stress plays an important role on the pathologies of cardiac remodeling. The aim of this study was to explore the influence of VD deficiency on cardiac oxidative stress and the potential sig?nal pathway. Methods The male C57 mice ( 3 weeks old) were randomly divided into three groups: vitamin D deficiency ( VDD ) group ( vitamin D deficiency feed for 10 weeks) , vitamin D deficiency ( VDA) group ( vitamin D sufficiency feed for 10 weeks) and VDD+calcitriol ( CAL) group ( vitamin D deficiency feed for 10 weeks and then vitamin D sufficiency feed and calcitriol treatment for 10 weeks) . Results There were significant differences between the VDD group and the VDA group in the left ventricular end?diastolic diameter and left ventricular mass index (3.82±0.125 mm vs 3.748±0.092 mm, P<0.05) (119.30±8.54 vs 97.60±3.65, P<0.05). The number of myocardial cells stained with 8?OHDG was higher in the VDD group compared with the VDA group ( 65. 4 ± 2. 3 vs 21. 8 ± 1. 6, P<0.05) whereas was lower after calcitriol supplement. Furthermore, the expression of thioredoxin interacting protein (TXNIP) was sig?nificantly up?regulated and the ratio of p?ASK?1/ASK?1, cytochrome C release, and caspase3 activation were increased in the VDD group . Conclusion VDD can lead to cardiac oxidative injury and the up?regulation of TXNIP and the activation of ASK?1 related apoptotic signal cascade may be involved in this procedure.
