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β-胡萝卜素对氧化应激和心脏连接蛋白 43 表达的影响。

Effect of beta-carotene on oxidative stress and expression of cardiac connexin 43.

出版信息

Arq Bras Cardiol. 2013 Sep;101(3):233-9. doi: 10.5935/abc.20130160. Epub 2013 Aug 6.

Abstract

BACKGROUND

Intervention studies have shown an increased mortality in patients who received beta-carotene. However, the mechanisms involved in this phenomenon are still unknown.

OBJECTIVE

Evaluate the influence of beta-carotene on oxidative stress and the expression of connexin 43 in rat hearts.

METHODS

Wistar rats, weighing approximately 100 g, were allocated in two groups: CONTROL GROUP (n=30), that received the diet routinely used in our laboratory, and Beta-Carotene Group (n = 28), which received beta-carotene (in crystal form, added and mixed to the diet) at a dose of 500 mg of beta-carotene/kg of diet. The animals received the treatment until they reached 200-250 g, when they were sacrificed. Samples of blood, liver and heart were collected to perform Western blotting and immunohistochemistry for connexin 43; morphometric studies, dosages of beta-carotene by high-performance liquid chromatography as well as reduced glutathione, oxidized glutathione and lipids hydroperoxides were performed by biochemical analysis.

RESULTS

Beta-carotene was detected only in the liver of Beta-Carotene Group animals (288 ± 94.7 µg/kg). Levels of reduced/oxidized glutathione were higher in the liver and heart of Beta-Carotene Group animals (liver -

CONTROL GROUP

42.60 ± 1.62; liver - Beta-Carotene Group: 57.40 ± 5.90; p = 0.04; heart: -

CONTROL GROUP

117.40 ± 1.01; heart - Beta-Carotene Group: 121.81 ± 1.32 nmol/mg protein; p = 0.03). The content of total connexin 43 was larger in Beta-Carotene Group.

CONCLUSION

Beta-carotene demonstrated a positive effect, characterized by the increase of intercellular communication and improvement of anti-oxidizing defense system. In this model, mechanism does not explain the increased mortality rate observed with the beta-carotene supplementation in clinical studies.

摘要

背景

干预研究表明,接受β-胡萝卜素治疗的患者死亡率增加。然而,涉及这一现象的机制仍不清楚。

目的

评估β-胡萝卜素对大鼠心脏氧化应激和连接蛋白 43 表达的影响。

方法

将约 100 克重的 Wistar 大鼠分为两组:对照组(n=30),给予我们实验室常规使用的饮食;β-胡萝卜素组(n=28),给予β-胡萝卜素(晶体形式,添加并混合到饮食中),剂量为 500mgβ-胡萝卜素/公斤饮食。动物接受治疗直至体重达到 200-250 克,然后处死。采集血液、肝脏和心脏样本,进行 Western 印迹和连接蛋白 43 免疫组织化学;进行形态学研究,通过高效液相色谱法测定β-胡萝卜素的剂量,以及通过生化分析测定还原型/氧化型谷胱甘肽、氧化型谷胱甘肽和脂质过氧化物氢。

结果

β-胡萝卜素仅在β-胡萝卜素组动物的肝脏中被检测到(288±94.7μg/kg)。β-胡萝卜素组动物的肝脏和心脏中还原型/氧化型谷胱甘肽水平升高(肝脏-对照组:42.60±1.62;肝脏-β-胡萝卜素组:57.40±5.90;p=0.04;心脏:-对照组:117.40±1.01;心脏-β-胡萝卜素组:121.81±1.32nmol/mg 蛋白;p=0.03)。β-胡萝卜素组总连接蛋白 43 的含量较大。

结论

β-胡萝卜素表现出积极的作用,表现为细胞间通讯增加和抗氧化防御系统改善。在这种模型中,机制并不能解释临床研究中观察到的β-胡萝卜素补充剂导致死亡率增加的现象。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32ff/4032303/994866955257/abc-101-03-0233-g01.jpg

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