Xin-ying Xu¹, Xi Yu², Zi-shan Liu², Qin-shuai Ni², Zhu-qin Yu^3,

Aim: To study the regulating effect and possible mechanism of Laminaria japonica polysaccharide (LJPS) on serum lipid in ApoE-/- mice of atherosclerostic hyperlipidemia. Methods: Twenty healthy male ApoE-/- mice were established atherosclerostic hyperlipidemia models by feeding with fat-rich diet for 12 weeks and and were randomly divided into model group and treated groups, ten healthy male C57BL/6J mice fed with ordinary feed as the control group. The mice in the treated group were gavaged LJPS once every other day for 4 weeks, while the mice in the control and model groups were simultaneously given equal volume saline. The serum levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol C (LDL-C) and high-density lipoprotein cholesterol C (HDL-C) were detected by biochemical assay. The activity of lipoprotein lipase (LPL) and hepatic lipase (HL) were determined by chemical colormetry. Enzyme-linked immunosorbent assay (ELISA) was applied to determine the level of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) and activity of HMG-CoA reducase (HMG-CR). The concentrations of malondialdehyde (MDA) and nitric oxide (NO) were respectively measured by thiobarbituric acid assay and nitrate reductase assay. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were respectively determined by xanthinoxidase assay and chemical colormetry. Results: After treated with LJPS, the body weights of mice in the treated group were significantly decreased than that in the model group (P<0.05), and the serum levels of TG, TC and LDL-C were significantly decreased (P<0.05) while the HDL-C was significantly increased (P<0.05) than those in the model group. In treated group mice, the activities of LPL and HL in serum and hepatic tissue were significantly higher than those in model group (P<0.05), while the HMG-CoA level of hepatic tissue was significantly higher and the HMG-CR activity lower than those in model group mice (P<0.05). In the model group mice, the levels of MDA and NO in serum and hepatic tissue were lower, while the activities of SOD and GSH-PX were significantly higher than those in the model group mice (P<0.05). Conclusion: It is suggested that LJPS could regulate the lipid metabolism by enhancing the activities of LPL and HL and inhibiting the activity of HMG-CR, and by increasing the activities of SOD and GSH-PX to reduce the levels of MDA and NO.

LJPS, lipids, atherosclerosis, LPL, HL, HMG-CR, MDA, NO, SOD, GSH-PX, ApoE-/- mice