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首页> 外文期刊>Journal of Cellular Physiology >Anionic nanoliposomes reduced atherosclerosis progression in Low Density Lipoprotein Receptor ( LDLR LDLR ) deficient mice fed a high fat diet
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Anionic nanoliposomes reduced atherosclerosis progression in Low Density Lipoprotein Receptor ( LDLR LDLR ) deficient mice fed a high fat diet

机译:阴离子nanoliposomes降低动脉粥样硬化发展在低密度脂蛋白受体(LDLR LDLR)不足的老鼠喂食高脂肪的饮食

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Atherosclerosis is a systemic disease characterized by the deposition of cholesterol and inflammatory cells within the arterial wall. Removal of cholesterol from the vessel wall may have an impact on the size and composition of atherosclerotic lesions. Anionic phospholipids or liposome vesicles composed of a lipid bilayer such as nanoliposomes have been suggested as treatments for dyslipidemia. In this study, we investigated the effect of anionic nanoliposomes on atherosclerosis in a mouse model. Low‐density lipoprotein receptor knockout mice ( Ldlr –/– ) were fed with an atherosclerosis promoting high fat and cholesterol (HFC) diet for 12 weeks. Anionic nanoliposomes including hydrogenated soy phosphatidylcholine (HSPC) and distearoyl phosphatidylglycerol (DSPG) (molar ratio: 1:3) were injected intravenously into HFC‐fed Ldlr ?/? mice once a week for 4 weeks. Mice receiving nanoliposomes had significantly reduced atherosclerosis within the aortic arch as assessed by Sudan IV staining area ( p ? =?0.007 ), and reduced intima/media ratio ( p ? =?0.030 ) and greater collagen deposition within atherosclerosis plaques within the brachiocephalic artery ( p ? =?0.007 ), compared to control mice. Administration of nanoliposomes enhanced markers of reverse cholesterol transport (RCT) and increased markers of plaque stability in HFC‐fed Ldlr ?/ ? mice. Reduced cholesterol accumulation was observed in the liver along with the up‐regulation of the major genes involved in the efflux of cholesterol such as hepatic ATP‐binding cassette transporters (ABC) including Abc‐a1 , Abc‐g1 , Abc‐g5 , and Abc‐g8 , Scavenger receptor class B, member 1 ( Scarb1 ), and Liver X receptor alpha ( Lxr )‐ α . Lecithin Cholesterol Acyltransferase activity within the plasma was also increased in mice receiving nanoliposomes. Anionic nanoliposome administration reduced atherosclerosis in HFC‐fed Ldlr ?/? mice by promoting RCT and upregulating the ABC‐A1/ABC‐G1 pathway.
机译:动脉粥样硬化是一种全身性疾病胆固醇的沉积特征和炎症细胞在动脉壁内。清除血管壁胆固醇的可能影响的大小和组成动脉粥样硬化病变。一个脂双分子层组成的脂质体囊泡已经提出nanoliposomes等血脂异常的治疗方法。研究阴离子nanoliposomes的效果在动脉粥样硬化小鼠模型。脂蛋白受体基因敲除小鼠(Ldlr - / -)喂养与动脉粥样硬化促进高吗脂肪和胆固醇(HFC)为12周的饮食。阴离子nanoliposomes包括氢化大豆磷脂酰胆碱(公司)和distearoylphosphatidylglycerol (DSPG)(摩尔比:1:3)静脉注射到氢氟烃量美联储Ldlr吗? / ?老鼠每周4周。nanoliposomes明显减少在主动脉弓动脉粥样硬化评估苏丹IV染色区(p ?),减少内膜/媒体比率(p ?和更大的胶原蛋白沉积动脉粥样硬化斑块内头臂动脉动脉(p ?控制老鼠。增强反向胆固醇运输的标志(RCT)和增加斑块稳定性的标记在氢氟烃检测——美联储Ldlr ? / ?观察积累在肝脏量调节的主要基因参与胆固醇,如肝的流出ATP结合盒转运蛋白(ABC)包括Abc‐a1, Abc‐太阳风暴,Abc‐g5和Abc‐g8, Scavenger受体B类,成员1 (Scarb1)和肝脏X受体α(Lxr)α。胆固醇酰基转移酶活动中等离子体在小鼠接受也增加了nanoliposomes。政府降低动脉粥样硬化在HFC的美联储Ldlr ? / ?《ABC》‐A1 / ABC‐太阳风暴pathway .

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