243 research outputs found

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

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    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 di

    Nonparametric Testing for Anomaly Effects in Empirical Asset Pricing Models

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    Ministry of Education, Singapore under its Academic Research Funding Tier

    Prostaglandin E2 receptor type 2-selective agonist prevents the degeneration of articular cartilage in rabbit knees with traumatic instability

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    [Introduction]Osteoarthritis (OA) is a common cause of disability in older adults. We have previously reported that an agonist for subtypes EP2 of the prostaglandin E2 receptor (an EP2 agonist) promotes the regeneration of chondral and osteochondral defects. The purpose of the current study is to analyze the effect of this agonist on articular cartilage in a model of traumatic degeneration. [Methods]The model of traumatic degeneration was established through transection of the anterior cruciate ligament and partial resection of the medial meniscus of the rabbits. Rabbits were divided into 5 groups; G-S (sham operation), G-C (no further treatment), G-0, G-80, and G-400 (single intra-articular administration of gelatin hydrogel containing 0, 80, and 400 μg of the specific EP2 agonist, ONO-8815Ly, respectively). Degeneration of the articular cartilage was evaluated at 2 or 12 weeks after the operation. [Results]ONO-8815Ly prevented cartilage degeneration at 2 weeks, which was associated with the inhibition of matrix metalloproteinase-13 (MMP-13) expression. The effect of ONO-8815Ly failed to last, and no effects were observed at 12 weeks after the operation. [Conclusions]Stimulation of prostaglandin E2 (PGE2) via EP2 prevents degeneration of the articular cartilage during the early stages. With a system to deliver it long term, the EP2 agonist could be a new therapeutic tool for OA
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