在长期地暴露的老鼠肝减少 LDL 受体和增加 angiotensinogen 基因表示的饮酒作乐乙醇吸入

• 作者: Annayya R Aroor Shivendra D Shukla
• 来源期刊: 世界肝病学杂志：英文版（电子版）
• 学科: 医学
• 关键词: ALCOHOLIC liver injury ANGIOTENSINOGEN Ethanol BINGE Extracellular regulated kinases1/2 LOW-DENSITY lipoproteun-receptor PLASMINOGEN activator inhibitor-1
• 年，卷（期）: 2011,（9）
• 页码范围: 250-255
• 页数: 6页
• 分类号: R575

摘要

AIM: To investigated the status of low-density lipoprotein (LDL)-receptor and angiotensionogen gene expression in rats treated chronically with ethanol followed by binge administration, a model that mimics the human scenario. METHODS: Rats were chronically treated with ethanol in liquid diet for 4 wk followed by a single binge mode of ethanol administration (5 mg/kg body weight). Samples were processed 4 h after binge ethanol administration (chronic ethanol binge). Control rats were fed isocaloric diet. In the control for binge, ethanol was replaced by water. Expression of mRNA for angioten-sinogen, c-fos and LDL-receptor, and nuclear accumulation of phospho-extracellular regulated kinases (ERK)1/2 and ERK1/2 protein were examined. RESULTS: Binge ethanol administration in chronically treated rats caused increase in steatosis and necrosis. Chronic ethanol alone had negligible effect on mRNA levels of LDL-receptor, or on the levels of nuclear ERK1/2 and phospho-ERK1/2. But, chronic ethanol followed by binge caused a decrease in LDL-receptor mRNA, and also decreased the levels of ERK1/2 and phospho-ERK1/2 in the nuclear compartment. On the other hand, chronic ethanol-binge increased mRNA expression of angiotensinogen and c-fos. CONCLUSION: Binge ethanol after chronic exposure, causes transcriptional dysregulation of LDL-receptor and angiotensinogen genes, both cardiovascular risk factors.