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Effect of Phosphatidylcholine Nanosomes on Phospholipid Composition of the Plasma Membranes in Liver Cells and Blood Serum in Experimental Atherosclerosis.
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- Additional Information
- Source:
Publisher: Springer Country of Publication: United States NLM ID: 0372557 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1573-8221 (Electronic) Linking ISSN: 00074888 NLM ISO Abbreviation: Bull Exp Biol Med Subsets: MEDLINE
- Publication Information:
Publication: New York : Springer
Original Publication: New York, Consultants Bureau.
- Subject Terms:
- Abstract:
Alimentary atherosclerosis is associated with a significant decrease in the content of phosphatidylcholine, the phospholipid that provides antioxidant protection, in the plasma membrane of liver cells, while the level of phosphatidic acid that initiates generation of superoxides, on the contrary, increases. The level of membrane phosphatidylserine, a target of the scavenger receptors, which initiates removal of damaged cells and modified lipoproteins from the circulation was also elevated. In the blood serum of rabbits receiving an atherogenic diet, the content of cardiolipin involved in the immune mechanisms of atherosclerosis development and a risk factor for thrombosis, sharply increased. The level of lysophosphatidylcholine that mediates initiation and progression of atherosclerosis increased. The content of phosphatidylinositol that is involved in the mechanisms protecting from exposure to excess cholesterol was significantly reduced. Treatment of alimentary atherosclerosis with "empty" phosphatidylcholine nanosomes eliminates the key factors initiating atherosclerosis development.
- Contributed Indexing:
Keywords: atherosclerosis; liver; phosphatidylcholine nanosomes; phospholipids; plasma membrane
- Accession Number:
0 (Antioxidants)
0 (Cardiolipins)
0 (Lipoproteins)
0 (Lysophosphatidylcholines)
0 (Phosphatidylcholines)
0 (Phospholipids)
- Publication Date:
Date Created: 20201202 Date Completed: 20211011 Latest Revision: 20211011
- Publication Date:
20231215
- Accession Number:
10.1007/s10517-020-05028-9
- Accession Number:
33263842
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