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高脂肪/高盐饮食对心肌氧化应激的影响。

Impact of high fat/high salt diet on myocardial oxidative stress.

机构信息

a Department of Clinical Pharmacy, Faculty of Pharmacy , Jordan University of Science and Technology , Irbid , Jordan.

出版信息

Clin Exp Hypertens. 2017;39(2):126-132. doi: 10.1080/10641963.2016.1226894. Epub 2017 Feb 28.

DOI:10.1080/10641963.2016.1226894
PMID:28287889
Abstract

BACKGROUND

High fat high salt diet contributes to oxidative stress and cardiac diseases.

AIMS

To determine the impact of moderately high fat diet (HFD), high salt (HS) or their combination on blood pressure (Bp) and myocardial oxidants/antioxidants.

METHODS

Sprague Dawley rats were assigned into four groups; conventional diet (control, 5% fat, 0.5% NaCl), HFD (25% fat, 0.5% NaCl), HS (5% fat, 8% NaCl), or combined diet (HFD+HS) for 10 weeks. Bp and cardiac oxidants and antioxidants were measured.

RESULT

HFD, HS, and their combination didn't cause obesity or dyslipidemia. Both HS and combined diets resulted in an increase in the heart/body weight ratio accompanied by an increase in Bp. No changes were observed in levels of the glutathione (GSH) system or superoxide dismutase (SOD) activities. However, a significant decrease in TBARS levels was observed in the HFD and the combined diet with a parallel increase in catalase activity in all groups. Relative to HFD, the combined diet was associated with increases in GSH reductase/peroxidase and SOD activities.

CONCLUSIONS

The lack of changes in the GSH system, the decrease in TBARS, and the increase in catalase activity suggest that normal hearts adapt compensatory mechanisms to prevent oxidative damage in response to HFD/and or HS.

摘要

背景

高脂肪高盐饮食会导致氧化应激和心脏疾病。

目的

确定适度高脂肪饮食(HFD)、高盐(HS)或它们的组合对血压(Bp)和心肌氧化剂/抗氧化剂的影响。

方法

将 Sprague Dawley 大鼠分为四组;常规饮食(对照组,5%脂肪,0.5% NaCl)、HFD(25%脂肪,0.5% NaCl)、HS(5%脂肪,8% NaCl)或联合饮食(HFD+HS),共 10 周。测量血压和心肌氧化剂和抗氧化剂。

结果

HFD、HS 和它们的组合并没有导致肥胖或血脂异常。HS 和联合饮食均导致心脏/体重比增加,同时血压升高。谷胱甘肽(GSH)系统水平或超氧化物歧化酶(SOD)活性没有变化。然而,HFD 和联合饮食组的 TBARS 水平显著降低,同时所有组的过氧化氢酶活性均增加。与 HFD 相比,联合饮食与 GSH 还原酶/过氧化物酶和 SOD 活性增加有关。

结论

GSH 系统没有变化,TBARS 减少,过氧化氢酶活性增加,这表明正常心脏会适应代偿机制,以防止氧化应激对 HFD/和或 HS 的损害。

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