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cholic acid/accident vasculaire cérébral

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Protective Effect of Cholic Acid-Coated Poly Lactic-Co-Glycolic Acid (PLGA) Nanoparticles Loaded with Erythropoietin on Experimental Stroke.

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Stroke is a major cause of adult mortality and morbidity worldwide. However, the treatment of stroke using the vast majority of possible drug candidates, including erythropoietin (EPO), remains problematic because of the presence of the blood-brain barrier (BBB), resulting in scarce penetration onto
Stroke is the second leading cause of death after heart disease globally and cerebral ischemic stroke accounts for approximately 70% of all incident stroke cases. We selected four main compounds from a patent Chinese medicine, Qingkailing (QKL) injection, including baicalin from Scutellaria

[Study on the glomerular foam cells in stroke-prone SHR].

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Recent evidence suggests focal glomerulosclerosis may be analogous to atherosclerosis. To investigate the role of hypertension and hypercholesterolemia in the appearance of glomerular foam cells, 2, 6 or 9-month-old stroke-prone SHR (SHRSP) were fed the high fat cholesterol diet (2% cholesterol,
The effect of the acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor HL-004 on bile acid production was studied during the regression phase of pre-established hypercholesterolemia in stroke-prone spontaneously hypertensive rats (SHRSP). These rats were fed a hypercholesterolemic diet containing

Reduced bile acid excretion is an independent risk factor for stroke and mortality: A prospective follow-up study.

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Hypercholesterolemia is a major risk factor for atherosclerosis, which is a cornerstone of coronary artery disease (CAD), stroke, peripheral vascular disease, aortic aneurysm and renal artery stenosis. This study investigated the association of bile acid excretion (BAE) with stroke

A possible role of chenodeoxycholic acid and glycine-conjugated bile acids in fibrotic steatohepatitis in a dietary rat model.

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OBJECTIVE Our previous study indicated that hepatic bile acids (BAs) may have deposited and stimulated the pathogenesis of a high fat-cholesterol (HFC) diet-induced fibrotic steatohepatitis in stroke-prone spontaneously hypertensive 5/Dmcr rats, based on dysregulated BA homeostasis pathways. We

Hypertension as an important factor for cerebrovascular atherogenesis in rats.

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A new model for studies on atherogenesis in the cerebrovascular system was obtained by using recently established stroke-prone spontaneously hypertensive rats (SHRSP). SHRSP on a hypercholesterolemic diet (20% suet, 5% cholesterol, and 2% cholic acid) had ring-like fat deposits in the circle of

Farnesoid X receptor represses hepatic human APOA gene expression.

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High plasma concentrations of lipoprotein(a) [Lp(a), which is encoded by the APOA gene] increase an individual's risk of developing diseases, such as coronary artery diseases, restenosis, and stroke. Unfortunately, increased Lp(a) levels are minimally influenced by dietary changes or drug treatment.

High susceptibility of obese hypertensive SHRSP.Z-Lepr(fa) /IzmDmcr rats to lipid deposition in the mesenteric artery.

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1. Atherosclerosis is commonly observed in obesity. Obese atherosclerosis-prone animals may be a promising tool for understanding the pathophysiology of obesity-associated atherosclerosis. However, most rat strains are resistant to atherosclerosis. The aim of the present study was to assess the

Bile acid-activated receptors in the treatment of dyslipidemia and related disorders.

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Dyslipidemia is a metabolic disorder that constitutes a major risk factor for cardiovascular diseases and stroke and is often associated with diabetes mellitus and atherosclerosis. In recent years a number of ligand-activated receptors have been found to exert a role in integrating essential steps

Hyodeoxycholic acid protects the neurovascular unit against oxygen-glucose deprivation and reoxygenation-induced injury in vitro.

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Calculus bovis is commonly used for the treatment of stroke in traditional Chinese medicine. Hyodeoxycholic acid (HDCA) is a bioactive compound extracted from calculus bovis. When combined with cholic acid, baicalin and jas-minoidin, HDCA prevents hypoxia-reoxygenation-induced brain injury by
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