| Summary: | 碩士 === 國立陽明大學 === 生物化學研究所 === 92 === Many previous studies indicated that fish oils and marine n-3 polyunsaturated fatty acids (PUFAs) have benefits with regard to the prevention of cardiovascular diseases. However, the mechanism contributing to the benefit of n-3 PUFAs has not been fully understood. In present study, we investigated the effect of different PUFAs on the redox status and lipid trafficking in apoE knockout mice and macrophages, respectively.
In animal experiment, forty apoE knockout mice were divided into five groups including the control, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA), and linoleic acid (LA) groups. After being fed by gavage for ten weeks, animals were sacrificed and specimens of blood, liver, and aorta were collected, respectively. There was no significant difference in plasma levels of total cholesterol, HDL-C, and LDL-C among groups of apoE knockout mice fed with AA, EPA, and DHA. However, plasma and liver levels of triglyceride were significantly increased in mice fed with LA. The levels of hepatic cuprozinc-superoxide dismutase (Cu,Zn-SOD) were significantly higher in mice fed with AA and DHA, but the levels of hepatic glutathione peroxidase and catalase activities did not show difference among groups. The mice treated with DHA had the least content of atherosclerotic lesions in the aorta, while the mice treated with LA had the most. In cellular study, treatment of AA, EPA, DHA, and LA decreased the cholesterol efflux in J774A.1 macrophages, but treatment of both PUFAs and 9-cis retinoic acid increased cholesterol efflux. There was no significant difference in cholesterol efflux and influx among groups of human primary macrophages treated with different PUFAs in the presence or absence of 9-cis retinoic acid.
Data from this study suggest that DHA may be the most active constituent of fish oils to prevent the process of atherosclerosis. DHA reduced the formation of atherosclerotic lesions in the aorta of apoE knockout mice probably via increasing SOD activity, not via lipid-lowering effect. However, we cannot rule out the involvement of other antiatherogenic mechanisms at present.
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