Hyperlipidemia Determines Dysfunctional HDL Production and Impedes Cholesterol Efflux in the Small Intestine: Alleviation by Ginger Extract
Hyperlipidemia Determines Dysfunctional HDL Production and Impedes Cholesterol Efflux in the Small Intestine: Alleviation by Ginger Extract
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DOI：
10.1002/mnfr.201900029
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发表时间：
2019-07-16
影响因子：
5.2
通讯作者：
Stancu, Camelia Sorina
中科院分区：
文献类型：
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作者：
Barbalata, Teodora;Deleanu, Mariana;Stancu, Camelia Sorina
范围评估生姜提取物（GIN）在刺激高质量HDL产生和小肠（SI）胆固醇流出方面的影响，这是高脂血症（HL）诱导的肝脂肪变性和动脉粥样硬化管理的关键过程。方法和结果使用三组仓鼠：（i）N，喂食标准饮食，（ii）HL，喂食高脂肪饮食21周，和（iii）HL-GIN，在饮食的最后5周用GIN处理HL。在血浆和SI中测量载脂蛋白A-I（apoA-I）、丙二醛-apoA-I（MDA-apoA-I）、对氧磷酶1（PON 1）和髓过氧化物酶（MPO）。在SI中评估ATP结合盒A1转运蛋白（ABCA 1）、ABCG 5/G8、肝脏X受体α/β（LXR α/β）、过氧化物酶体增殖物激活受体γ（PPAR γ）和沉默调节蛋白1（SIRT 1）。结果表明，GIN可降低HL血浆中MDA-apoA-I、MPO/PON 1比值，升高HDL-胆固醇/总胆固醇。在HL-SI中，GIN降低MDA-apoA-I和MPO，增加ApoA-I、PON 1和ABCA 1，并恢复HL干扰的胆固醇流出（SIRT 1-LXR α/β-PPAR γ-ABCG 8）。GIN给药与主动脉瓣脂质沉积减少相关。结论GIN可通过抑制氧化应激，恢复apoA-I的质量和数量，促进HL大鼠功能性HDL的合成，增加SI的胆固醇流出。这些作用与SIRT 1-LXR α/β-PPAR γ通路的恢复有关。
Scope To assess the impact of ginger extract (GIN) in stimulating the production of quality HDL and the cholesterol efflux in the small intestine (SI), key processes in the management of hyperlipidemia (HL)-induced hepatic steatosis, and atherosclerosis. Methods and results Three groups of hamsters are used: (i) N, fed standard diet, (ii) HL, fed high-fat diet for 21 weeks, and (iii) HL-GIN, HL treated with GIN for the last 5 weeks of diet. Apolipoprotein A-I (apoA-I), malondialdehyde-apoA-I (MDA-apoA-I), paraoxonase1 (PON1), and myeloperoxidase (MPO) are measured in plasma and SI. ATP-binding cassette A1 transporter (ABCA1), ABCG5/G8, liver X receptor alpha/beta (LXR alpha/beta), peroxisome proliferator-activated receptor gamma (PPAR gamma), and sirtuin1 (SIRT1) are assessed in the SI. Results show that in HL plasma, GIN decreases MDA-apoA-I, MPO/PON1 ratio and increases HDL-cholesterol/total cholesterol. In HL-SI, GIN decreases MDA-apoA-I and MPO, increases ApoA-I, PON1, and ABCA1, and restores cholesterol efflux disturbed by HL (SIRT1-LXR alpha/beta-PPAR gamma-ABCG8). GIN administration is associated with the reduction of the aortic valves lipid-deposits. Conclusion In HL conditions, GIN stimulates the functional HDL production by restoring apoA-I quality and quantity through inhibition of the oxidative stress, and increases cholesterol efflux in the SI. These effects are associated with the restoration of SIRT1-LXR alpha/beta-PPAR gamma pathway.