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机构地区:[1]解放军第三军医大学新桥医院急救部,重庆400037
出 处:《中国医药导报》2017年第2期20-24,共5页China Medical Herald
摘 要:目的探讨脂蛋白酯酶在compound K调节血脂水平中的作用。方法 36只雄性SD大鼠随机分为6组,除对照组外均给予高脂饮食,对照组和模型组给予生理盐水腹腔注射,compound K给药组分别给予compound K 1、3、9 mg/kg腹腔注射,GGPP组同时给予compound K 3、9 mg/kg GGPP。4周后处死动物,取样测定血脂、肝素后脂蛋白酯酶活性、脂蛋白酯酶表达水平等;培养大鼠肝细胞株BRL,分别给予compound K 3、10、30μmol/L处理12 h后,检测脂蛋白酯酶表达水平。结果与模型组比较,compound K 3、9 mg/kg组的总胆固醇、低密度脂蛋白胆固醇、三酰甘油显著降低,高密度脂蛋白胆固醇、肝素后血清脂蛋白酯酶活性和脂蛋白酯酶表达量显著增高,差异有统计学意义(P<0.05),且呈剂量依赖性。体外细胞试验结果与动物实验一致。结论 compound K能够通过增加脂蛋白酯酶的表达和活性达到降低高脂饮食大鼠血清三酰甘油的作用,其机制与compound K激活肝X受体α相关。Objective To explore the role of lipoprotein lipase (LPL) on serum lipid modulation of compound K. Methods 36 male SD rats were divided into 6 groups. All animals were fed with high fat diet except control group. Control group and model group were given intraperitoneal injection of saline, compound K groups were treated with different doses of compound K (1, 3, 9 mg/kg). GGPP group was administrated with compound K 3 and 9 mg/kg GGPP simultaneously. After 4 weeks, animals were sacrificed. Serum lipid profile, LPL activity and the expression of LPL mRNA and protein were measured. BRL cells were treated with different doses of compound K (3, 10, 30 μmol/L) for 12 h, and the expres- sion levels of LPL were measured. Results Compared with model group, total cholesterol, low-density lipoprotein cholesterol and triglycerides levels of compound K 3 and 9 mg/kg groups were significantly decreased, high density lipoprotein cholesterol, serum lipoprotein lipase activity after heparin and LPL expression of compound K 3 and 9 mg/kg groups were significantly increased, with statistical differences (P 〈 0.05), and the action depended on its dose. The re- suits of in vitro cell experiments were consistent with animal experiments. Conclusion compound K can reduce the ex- pression of serum triglyceride via up-regulation of LPL expression and activity, and the mechanism is associated with compound K activated liver X receptor a.
关 键 词:COMPOUND K 动脉粥样硬化 脂蛋白酯酶 肝x受体a
分 类 号:R543[医药卫生—心血管疾病]
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