白藜芦醇对高脂血症大鼠血小板聚集的影响及其机制研究

Study of the effects and the mechanism of resveratrol on platelet aggregation in hyperlipidemia rats

目的:研究白藜芦醇对高脂血症大鼠血小板聚集的影响及其可能机制。方法:建立大鼠的高脂血症模型,同时连续i.g.给予白藜芦醇(50mg.kg-1.d-1)或空白溶媒30d,测定大鼠血浆TC、TG、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、丙二醛(MDA)、超氧化物歧化酶(SOD)、NO、内皮一氧化氮合酶(eNOS)、P-选择蛋白、血栓烷B2(TXB2)和6-酮-前列腺素F1α(6-Keto-PGF1α),ADP诱导的血小板5 min最大聚集率。结果:与高脂模型组比较,高脂饲料白藜芦醇组大鼠在连续i.g.给予白藜芦醇(50mg.kg-1.d-1)30d后,大鼠血浆TG、TC、LDL-C含量均下降,分别下降19%、31%、51%,HDL-C含量增加1.33倍;SOD和eNOS活力升高,NO和6-Keto-PGF1α含量增加,MDA、P-选择蛋白、TXB2含量降低,ADP诱导的血小板5min最大聚集率降低。结论:白藜芦醇能有效降低血小板聚集,可能是通过降低血脂水平,防止脂质过氧化和保护内皮细胞完整,影响NO合成,维持血浆或组织中的TXA2和PGI2平衡及细胞内外的钙离子平衡等多环节来发挥作用。

Abstract： Abstract： Aim To explore the effects and the mechanism of resveratrol on platelet aggregation in hyperlipidemia rats. Methods Experimental hyperlipidemia rats were ig administration of resveratrol （50mg·kg^-1·d^-1） or vehicle in 30 d. The levels of plasma triplyceride （TG）, total cholesterol （TC）, high density lipoprotein cholesterol （HDL-C）, low density lipoprotein cholesterol （LDL-C）, malondialdehyde （MDA）, superoxide dismutase （SOD）,nitric oxide （NO）, endothelial nitric oxide synthase （eNOS）, granulemembrane protein-140（GMP-140）,thromboxaneB2 （TXB2）,6-keto –prostaglandin F1α （6-keto-PGF1α） and platelet maximal aggregation rate（MAR）which was induced by ADP in 5 minute were measured. Results Plasma TG, TC,LDL-C and HDL-C of the rats fed high fat diet （HFD） and ig resveratrol （50mg/kg？d） was 19%, 31%,51% lower and1.33times higher than that of the HFD group rats. The activity of SOD and eNOS in resveratrol and HFD group was higher （P〈0.01） and The content of NO and 6-keto-PGF1α in resveratrol and HFD group was higher （P〈0.01） and the MDA、 GMP-140、TXB2 and MAR in resveratrol and HFD group was lower than that of the HFD group （P〈0.05）. Conclusion Platelet aggregation rate was descreased in experimental hyperlipidemia rats by i.g. administration of resveratrol. its mechanism closely correlates with decline of plasma lipid and anti-peroxide of lipid and protecting vasoendothelial cells and improving the synthesis of NO as well as Keeping the balance of TXA2and PGI2 in tissue or plasma and the balance between extracellular calcium and intracellular calcium.