Salvianolic acid B Relieves Oxidative Stress in Glucose Absorption and Utilization of Mice Fed High-Sugar Diet

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...

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Veröffentlicht in:Tropical journal of pharmaceutical research 2016-06, Vol.13 (3), p.369
Hauptverfasser: Wang, Bin, Wang, Shuping, Sun, Jin, Shi, Yonghui, Le, Guowei
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Sprache:eng
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Zusammenfassung: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.
ISSN:1596-5996
1596-9827
DOI:10.4314/tjpr.v13i3.9