[Adiponectin in normal and atherosclerotic intima of human aorta]. / Adiponektin v normal'noi i ateroskleroticheski izmenennoi intime aorty cheloveka.

BACKGROUND: Adiponectin (AN) is a protein synthesized by adipocytes that has regulatory effects on lipid and lipoprotein metabolism, increases tissue sensitivity to insulin, and modulates endothelial functions and inflammatory response. However, its involvement in the processes of atherogenesis remains poorly understood. OBJECTIVE: To determine the localization and sources of AN in atherosclerotic and normal human aortic intima. MATERIAL AND METHODS: Immunohistochemical study was performed on sections of atherosclerotic and normal human aorta obtained during autopsy. Reverse transcription real-time PCR was performed using biopsies of para-aortic and abdominal adipose tissue, intima-media of the thoracic aorta, atherosclerotic plaques of the human carotid and femoral arteries, as well as on endothelial cells isolated from the human thoracic aorta. Transendothelial transport of AN was evaluated in a two-chamber model using a monolayer of human endothelial cell hybridoma EA.Hy926. RESULTS: It has been established that AN is present in atherosclerotic but not in normal human aortic intima. At the same time, AN ADIPOQ mRNA was not detected either in the intima media of the human aorta, nor in isolated endothelial cells of the aorta, nor in cells of atherosclerotic plaques of the carotid and femoral arteries. AN slowly penetrated the endothelial monolayer in vitro, but this transport was significantly enhanced by the action of tumor necrosis factor-alpha (TNFa). CONCLUSION: Obtained data indicate that AN is present in atherosclerotic but not in normal aortic intima. We assume that AN is not synthesized by the cells of normal and atherosclerotic arterial walls, but permeates from the plasma. Transendothelial transport of AN, like many other plasma proteins, is activated during the development of atherosclerotic lesions, apparently under the action of pro-inflammatory cytokines, in particular, TNFα.

[Molecular mechanisms of the cytoprotector cramizol effect in the experimental dyslipidemia model]. / Molekuliarnye mekhanizmy gipolipidemicheskogo deistviia tsitoprotektora kramizola pri éksperimental'noi dislipidemii.

The tested drug cramizol exhibits lipid-lowering and anti-atherogenic effects. Cramizol reduces blood cholesterol and triglycerides. It also increases HDL and reduces the atherogenic index in rats with the chronic dyslipidemia model induced by a hypercholesterol diet. Cramizol is effective as a hypolipidemic agent and its efficiency is comparable with the reference drug, phenofibrate. Cramizol increases expression of the ApoA1 and ApoC2 genes, and also reduces expression of the Scarb1 gene in rats with experimentally induced hyperlipidemia. These mechanisms could be the basis of its hypolipidemic and anti-atherogenic actions.

[Effects of сramizol on expression of the ApoA1 gene in rats with experimental hyperlipidemia]. / Vliianie kramizola na ékspressiiu gena apolipoproteina A1 (ApoA1) v pecheni krys pri éksperimental'no indutsirovannoi giperlipidemii.

An imidazole derivative cramizol, has lipid-lowering and anti-atherogenic effects. Cramizol reduces blood levels of cholesterol and triglycerides, and also reduces the atherogenic index in animals with acute hyperlipidemia induced by Triton WR-1339. Cramizol and the lipid-lowering drug fenofibrate exhibited similar effectiveness as hypolipidemic agents. Cramizol also restores the expression of the Apoa1 gene in rats with experimentally induced hyperlipidemia to normal values. This may be a basis of its hypolipidemic and anti-atherogenic action.