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降低血液致动脉粥样硬化性的方法。

Approach to reduction of blood atherogenicity.

作者信息

Orekhov Alexander N, Melnichenko Alexandra A, Sobenin Igor A

机构信息

Institute for Atherosclerosis Research, Skolkovo Innovation Center, P.O. Box No. 21, Moscow 121609, Russia ; Institute of General Pathology and Pathophysiology, Baltiyskaya Street 8, Moscow 125315, Russia.

Institute for Atherosclerosis Research, Skolkovo Innovation Center, P.O. Box No. 21, Moscow 121609, Russia ; Institute of General Pathology and Pathophysiology, Baltiyskaya Street 8, Moscow 125315, Russia ; Russian Cardiology Research and Production Center, 3rd Cherepkovskaya Street 15a, Moscow 121552, Russia.

出版信息

Oxid Med Cell Longev. 2014;2014:738679. doi: 10.1155/2014/738679. Epub 2014 Jun 29.

DOI:10.1155/2014/738679
PMID:25101152
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4101215/
Abstract

We have earlier found that blood sera of patients with coronary heart disease (CHD) increase lipid levels in cells cultured from subendothelial intima of human aorta. We have also revealed that the ability of blood sera to raise intracellular cholesterol; that is, their atherogenicity is caused by at least modified low density lipoprotein (LDL) circulating in the blood of patients and autoantibodies to modified LDL. In the present work we have demonstrated significant impact of nonlipid factor(s) to blood atherogenicity. We have developed an approach to removal of nonlipid atherogenicity factor(s) from blood serum based on the use of immobilized LDL. This approach was used for extracorporeal perfusion of patient's blood through the column with immobilized LDL. Pilot clinical study confirmed the efficacy of this approach for prevention of coronary atherosclerosis progression.

摘要

我们之前发现,冠心病(CHD)患者的血清会使源自人类主动脉内膜下层的培养细胞中的脂质水平升高。我们还发现,血清升高细胞内胆固醇的能力,即其致动脉粥样硬化性,至少是由患者血液中循环的修饰低密度脂蛋白(LDL)和针对修饰LDL的自身抗体引起的。在目前的工作中,我们证明了非脂质因子对血液致动脉粥样硬化性有显著影响。我们开发了一种基于使用固定化LDL从血清中去除非脂质致动脉粥样硬化因子的方法。该方法用于通过装有固定化LDL的柱子对患者血液进行体外灌注。初步临床研究证实了该方法在预防冠状动脉粥样硬化进展方面的有效性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d427/4101215/7c540f8301ed/OMCL2014-738679.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d427/4101215/277c48226403/OMCL2014-738679.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d427/4101215/7c540f8301ed/OMCL2014-738679.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d427/4101215/277c48226403/OMCL2014-738679.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d427/4101215/7c540f8301ed/OMCL2014-738679.002.jpg

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