中文摘要：

目的研究植酸钠对饮食所致高脂血症大鼠心血管保护作用机制。方法5周龄的Wistar大鼠按体重随机分成4组：正常饮食组（对照组）、高脂饮食组（高脂模型对照组）、高脂饮食＋100mg／kg植酸钠（高剂量植酸钠组）、高脂饮食＋50mg／kg植酸钠（低剂量植酸钠组）。4周后测定各组大鼠血脂、氧化应激、心肌瘦素、心肌Na^＋，K^＋-ATPase和Ca^2＋，Mg^2＋-ATPase酶水平。结果与对照组相比，高脂血症显著提高血清总胆固醇、甘油三脂、高密度脂蛋白、低密度脂蛋白的含量，提高血清丙二醛（MDA）水平，显著降低血清超氧化物岐化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）、过氧化氢酶（CAT）3种抗氧化酶水平，降低心肌Na^＋，K^＋-ATPase、Ca^2，Mg^2＋-ATPase和瘦素水平；高剂量或低剂量植酸钠组均可显著升高血清SOD、GSH—Px、CAT抗氧化酶水平，增高心肌Na^＋，K^＋-ATPase、Ca^2＋，Mg^2＋-ATPase水平，降低MDA含量，但对血脂水平无显著影响。高剂量植酸钠组还可显著增加心肌瘦素水平。结论植酸钠具有心血管保护作用，其作用机制至少包括抗氧化作用和增加心肌细胞的瘦素表达两个方面。

英文摘要：

Objective To study the possible mechanisms of cardiovascular protective effects of sodium phytase in diet-induced hyperlipoidemia rats. Methods Five-week old Wistar rats were fed with basic control diet （control group）, high fat diet （hyperlipoidemia group）, high fat diet plus sodium phytase 50 mg/kg body weight every day （oral garage, low dose group）, and high fat diet plus sodium phytase 100 mg/kg body weight every day （oral garage, high dose group） for 4 weeks. Lipid profile, oxidative stress status, leptin level in heart tissue, and cardiac Na^＋ , K^＋-ATPase and Ca^2＋ , Mg^2＋-ATPase activities were assessed. Results After treatment for 4 weeks, hyperlipoidemia was induced in rats fed with high fat diet. Compared with control group, the rats with hyperlipoidemia had higher plasma oxidative stress level, lower cardiac leptin level, and lower cardiac Na^＋ , K^＋-ATPase and Ca^2＋ , Mg^2＋ -ATPase activity （P〈0.05）. Sodium phytase supplementation protected cardiovascular system by increasing cardiac Na^＋ , K^＋-ATPase and Ca^2＋ , Mg^2＋-ATPase activities. Accompanying these protective effects, sodium phytase decreased plasma oxidative stress level and increased cardiac leptin level. But sodium phyatse had no hypoleptinemia or hypolipoidemia effect. Conclusion The mechanisms of anti-atherosclerotic effects of sodium phytase in diet-induced hyperlipoidemia rats included at least two aspects： increasing the sensitivity of hearts to leptin regulation by up-regulating the cardiac leptin expression and decreasing plasma oxidative stress level.