Mechanisms involved in the antiplatelet activity of lycopene

• Main Author: 王英
• Other Authors: 許準榕
• Format: Others
• Language: zh-TW
• Published: 2003
• Online Access: http://ndltd.ncl.edu.tw/handle/31274719641106466470

碩士 === 臺北醫學大學 === 醫學研究所 === 91 === Lycopene is a natural pigment that belongs to b-carotene, which is abundant in natural foods like tomatoes, watermelons, guavas, grapefruits, and so on. It’s molecular formula is C40H56; molecular weight is 537, and the structure is a kind of hydrocarbon compounds. Lycopene plays an important role in the scavenging of free radicals. It not only can delay human ageing, but also has been convinced for it’s effects on cancer prevention. Lycopene can decrease the risks of prostate cancer, breast cancer, lung cancer, and so on. During the process of platelet aggregation, there are free radicals produced which further strengthen the platelet activation. Therefore, the purpose of the study is to see if lycopene can inhibit platelet aggregation through it’s effects on free radicals and further to find the mechanisms involved in. In this study, we found that (1) the activated lycopene could effectively inhibit the platelet aggregation. Lycopene dose-dependently inhibited the aggregation induced by collagen, ADP and AA , the IC50 concentration is about 6 mM. (2) Lycopene significantly inhibited the intracellular Ca2+ mobilization and PI breakdown stimulated by collagen. (3) Lycopene increased the cGMP and NO formation in human platelets. In addition, lycopene also decreased the formation of TxB2, and the intracellular pH values. (4) Lycopene also significantly inhibited platelet aggregation and decreased the 47 kDa protein phosphorylation induced by PDBu, an PKC activator. Therefore, basing on the above observations, we suggest that the possible mechanisms maybe involved as follows : (1) Lycopene inhibited phospholipase C, and then inhibited the phosphoinositide breakdown, 47 kDa protein phosphorylation and formation of TxA2. (2) On the other hand, lycopene increased the amount of NO and c-GMP by activating guanylate cyclase. Through the effects of (1) and (2), the intracellular Ca2+ concentration was decreased finally and leading to the inhibition of platelet aggregation.