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首页> 外文期刊>Journal of pharmacological sciences. >Hypolipidemic mechanisms of Ananas comosus L. leaves in mice: different from fibrates but similar to statins.
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Hypolipidemic mechanisms of Ananas comosus L. leaves in mice: different from fibrates but similar to statins.

机译:小鼠凤梨叶片的降血脂机制:与贝特类药物不同,但与他汀类药物相似。

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In this study, we investigated hypolipidemic mechanisms of the ethanolic extract of Ananas comosus L. leaves (AC) in mice and then determined its activities in related enzymes. The results showed that AC (0.40 g/kg) significantly inhibited the increase in serum triglycerides by 40% in fructose-fed mice. In mice induced by alloxan and high-fat diets, serum total cholesterol remained at a high level (180 - 220 mg/dl) within 7 days of removing high-fat diets but reached normal level (120 - 140 mg/dl) after AC (0.40 g/kg per day) treatment. Also, AC (0.40 and 0.80 g/kg) significantly inhibited serum lipids from the increase in Triton WR-1339-induced hyperlipidemic mice. AC (0.01 - 100 microg/ml) selectively activated lipoprotein lipase (LPL) activity by 200% - 400% and significantly inhibited 3-hydroxyl-methyl glutaryl coenzyme A (HMGCoA) reductase activity by 20% - 49% in vitro. Furthermore, 2 months of fenofibrate (0.20 g/kg) administration particularly increased mice liver weights (0.0760 +/- 0.0110 g/g) while AC (0.40 g/kg) had no effect (0.0403 +/- 0.0047). Taken together, these results suggest that AC will be a new potential natural product for the treatment of hyperlipidemia that exerts its actions through mechanisms of inhibiting HMGCoA reductase and activating LPL activities. Its action mechanisms differentiate from those with fibrates but may be partly similar to those with statins. It is hopeful that AC may serve as the adjuvant for fibrates.
机译:在这项研究中,我们调查了凤梨叶片(AC)小鼠乙醇提取物的降血脂机制,然后确定了其在相关酶中的活性。结果表明,在果糖喂养的小鼠中,AC(0.40 g / kg)显着抑制了血清甘油三酸酯的增加40%。在四氧嘧啶和高脂饮食诱导的小鼠中,去除高脂饮食后7天内血清总胆固醇保持在高水平(180-220 mg / dl),但在AC后达到正常水平(120-140 mg / dl) (每天0.40 g / kg)治疗。同样,AC(0.40和0.80 g / kg)显着抑制了Triton WR-1339诱导的高脂血症小鼠的血脂。在体外,AC(0.01-100 microg / ml)选择性激活脂蛋白脂肪酶(LPL)活性200%-400%,并显着抑制3-羟基-甲基戊二酰辅酶A(HMGCoA)还原酶活性。此外,给予非诺贝特(0.20 g / kg)2个月特别增加了小鼠的肝脏重量(0.0760 +/- 0.0110 g / g),而AC(0.40 g / kg)没有作用(0.0403 +/- 0.0047)。综上所述,这些结果表明AC将成为治疗高脂血症的一种新的潜在天然产物,它通过抑制HMGCoA还原酶和激活LPL活性的机制发挥作用。它的作用机制不同于那些有贝特类药物的作用机制,但可能部分与他汀类药物的作用机制相似。希望AC可以作为贝特类的佐剂。

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