Abstract
Purpose : To evaluate the influence of Salvianolic acid B (Sal B) on oxidative stress in mice administrated with glucose, sucrose and high-sugar diet. Methods : 40 Kunming mice were divided into four groups of 10. After a fast of 12 h, mice were treated by oral infusion respectively with physiological saline, 20 % glucose, 20 % sucrose, and 20 % glucose + 0.002 % Sal B. Blood glucose and levels of reactive oxygen species (ROS) were determined at 0, 0.5, 1.0, 1.5, and 2.0 h after administration. Another 3 groups of 10 Kunming mice each were fed with normal diet, high-sugar diet (20 % sucrose, HSD) and HSD + 0.002 % Sal B. Four weeks later, the levels of ROS as well as antioxidant enzyme activity were determined. Results : Blood ROS showed the first peak at 0.5 h and a higher peak at 1.5 h after high glucose administration. ROS were mainly produced in liver and pancreas with the utilization of glucose. Sal B administration prevented increase in blood glucose and significantly (p < 0.05) reduced ROS produced in the process of glucose absorption and utilization, especially the latter. Sal B decrease oxidative stress induced by HSD through scavenging ROS associated with increased activity of antioxidant enzymes. Conclusion : This study demonstrates that Sal B can decrease oxidative stress in glucose absorption and utilization in HSD mice. Thus, the findings provide a basis for a potential interventional strategy for protecting against oxidative damage induced by HSD. Keywords : Salvianolic acid B, Blood glucose, Reactive oxygen species, Oxidative stress, Sugar die
Highlights
Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the scavenging ability of antioxidants [1]
Cumulative evidence showed that oxidative stress, induced by reactive oxygen derived from hyperglycemia, caused abnormal gene expression, altered signal transduction as well as the activation of pathways leading to programmed myocardial cell deaths [5]
We found that Salvianolic acid B (Sal B) administration did not change the trend of ROS and blood glucose in high glucose administrated mice, but reduced the level of ROS, especially in the utilization of glucose (p < 0.05) and prevented the increase of blood glucose (p > 0.05) (Fig 2A and B)
Summary
Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the scavenging ability of antioxidants [1]. Emerging evidence indicates that excessive production of ROS is an important factor that contributes to the pathophysiology of a variety of diseases. Hyperglycemia is a widely known cause of enhanced free radical concentration, which can generate free radicals by autoxidation and glycation of proteins [3]. Elevated glucose concentration directly injures cells and induces lipid peroxidation, which is the main cause for diabetic complications [4]. Cumulative evidence showed that oxidative stress, induced by reactive oxygen derived from hyperglycemia, caused abnormal gene expression, altered signal transduction as well as the activation of pathways leading to programmed myocardial cell deaths [5]
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