Vitis labrusca Extract (HP01) Improves Blood Circulation and Lipid Metabolism in Hyperlipidemic Rats

• Main Authors: Bo Yoon Chang, Dae Sung Kim, Sung Yeon Kim
• Format: Article
• Language: English
• Published: Hindawi Limited 2020-01-01
• Series: Evidence-Based Complementary and Alternative Medicine
• Online Access: http://dx.doi.org/10.1155/2020/6180310

Excessive intake of high-lipid foods and lifestyle changes can easily cause hyperlipidemia. Hyperlipidemia is clinically considered a major risk factor for cardiovascular disease, which is the second leading cause of death worldwide. In this study, the effects of a Vitis labrusca extract (HP01) on coagulation, platelet aggregation, and lipid metabolism were investigated in hyperlipidemic rats. A rat model of high-fat diet- (HFD-) induced hyperlipidemia was used. Hemostatic parameters and lipid levels were investigated after HP01 treatment of hyperlipidemic rats. Different doses of HP01 (200 mg/kg/day and 400 mg/kg/day, p.o.) were administered for 3 weeks, and prothrombin time (PT), activated partial thromboplastin time (aPTT), and platelet aggregation and bleed time (BT) were determined. The levels of thromboxane B(2) (TXB(2)) and serotonin were measured using enzyme-linked immunosorbent assay kits. Simultaneously, hepatic function and blood fat indexes, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), malondialdehyde (MDA), and glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were also measured. In comparison with the data obtained for rats in the untreated HFD group, HP01 (200 mg/kg) treatment prolonged PT but did not affect aPTT. HP01 treatment did not alter plasma TXB(2), PGI2, or serotonin levels. However, HP01 showed some effects in improving liver function by reducing the levels of hepatic lipids. ALT, MDA, and hepatic TG levels significantly decreased, whereas GSH, GPx, CAT, and SOD levels significantly increased. These results confirm the HP01 extract will improve thromboplastic and the liver metabolic disorders in hyperlipidemia by oxidative stress response.