原花青素对饮食所致高脂血症大鼠心血管的保护作用

[目的]研究原花青素对饮食所致高脂血症大鼠心血管的保护作用机制.[方法]对5周龄Wistar大鼠按体重随机分成4组:正常饮食组(对照组,C组)、高脂饮食组(高脂模型对照组,H组)、高脂饮食 20mg/ks原花青素(药物高剂量,HD组)、高脂饮食 10 mg/kg原花青素(低剂量组,LD组).喂饲4周后测定各组大鼠血脂、氧化应激和心肌瘦素、Na -K -ATPase酶和ca2-Mg2 -ATPase酶水平.[结果]与对照组相比,H组血清总胆固醇(CHO)、三酰甘油(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)及丙二醛(MDA)水平显著升高,血清SOD、GSH-Px、CAT三种抗氧化酶水平明显降低,心肌Na -K -ATPase酶、Ca2 -Mg2 -ATPase酶和MDA水平降低;HD和LD组血清SOD、GSH-Px、CAT以及心肌Na K -ATPase酶、ca2 -Mg2 -ATPase酶和瘦素水平显著升高,MDA含量降低,但对血脂水平无显著影响.[结论]原花青素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对瘦素的调节敏感性两个方面.

Cardiovasular Protective Effect of Proanthocyanidins in Diet-induced Hyperfipoidemia Rats

Objective To study the possible mechanisms of cardiovascular protective effects of proanthocyanidins in diet-induced hyperlipoidemia rats. Methods 5-week old Wistar rats were fed with basic diet(control group),high fat diet (hyperlipoidemia group),high fat diet proanthocyanidins 10 mg/kg body weight/day(oral gavage,low dose group),and high fat diet proanthocyanidins 20 mg/kg body weight/day(oral gavage,high dose group)for 4 weeks. Lipid profile,oxidative stress status,leptin level in heart tissue,cardiac Na ,K -ATPase and Ca2 ,Mg2 -ATPase activities were assessed. Results After 4-weeks treatment,hyperlipoidemia was induced in rats fed with high fat diet. Compared with control group,hyperlipoidemia rats had higher plasma oxidative stress level,lower cardiac leptin level,lower cardiac Na ,K -ATPase and Ca2 ,Mg2 -ATPase activity(P < 0.05). Proanthocyanidins supplementation protected cardiovascular system by increasing cardiac Na ,K -ATPase and Ca2 ,Mg2 -ATPase activities. Accompanying these protective effects,proanthocyanidins decreased plasma oxidative stress level. At the same time,proanthocyanidins enhanced cardiac sensitivity to leptin regulation by increasing cardiac leptin. But sodium phyatse had no hypoleptinemia or hypolipoidemia effect. The cardiovascular protective effects of proanthocyanidins in diet induced hyperlipoidemia rats included at least two aspects:increased cardiac leptin expression,and decreased plasma oxidative stress level.