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目的探讨炎症对清道夫受体A(scavenger receptor A,SRA)和CD36双基因敲除(SRA-/-/CD36-/-)小鼠肝脏LDL受体表达的影响及其潜在机制。方法将1~3月龄,体质量为18~23g的SRA-/-/CD36-/-雄性小鼠随机分为对照组(n=7),炎症组(n=6),2组均喂以高脂饮食,炎症组小鼠采取皮下注射酪蛋白方法诱导产生慢性炎症模型,14周后应用实时荧光定量RT-PCR技术和免疫组化方法检测肝脏LDL受体基因及调控其转录的SREBP2、SCAP基因表达水平,并观察肝脏形态学及血生化指标的变化。结果与正常对照相比,炎症状态时肝脏LDL受体、SREBP2、SCAP mRNA水平显著高于对照组(P<0.05),蛋白表达的水平也较对照组明显升高;肝细胞内脂质沉积加重,炎性细胞浸润;血清总胆固醇和低密度脂蛋白胆固醇水平均明显降低(P<0.05),高密度脂蛋白胆固醇、甘油三酯降低不明显。结论炎症通过促进肝细胞内SREBP2、SCAP的表达,进而增强细胞膜表面LDL受体的表达,最终导致肝细胞内胆固醇沉积。
Objective To investigate the effects of inflammation on the expression of liver LDL receptor in scavenger receptor A (SRA) and CD36 double knockout (SRA - / - / CD36 - / -) mice and its potential mechanism. Methods SRA - / - / CD36 - / - male mice aged 1-3 months and 18-23g were randomly divided into control group (n = 7) and inflammation group (n = 6) The model of chronic inflammation was induced by subcutaneous injection of casein in a high-fat diet and inflammation group. After 14 weeks, liver LDL receptor gene and SREBP2 gene were detected by real-time fluorescence quantitative RT-PCR and immunohistochemistry. SCAP gene expression levels, and observe the liver morphology and blood biochemistry changes. Results Compared with the normal control group, the levels of LDL receptor, SREBP2 and SCAP mRNA in the liver were significantly higher than those in the control group (P <0.05), and the protein expression levels were significantly higher than those in the control group. The lipid deposition in the hepatocytes increased , Inflammatory cell infiltration; serum total cholesterol and low density lipoprotein cholesterol levels were significantly lower (P <0.05), high-density lipoprotein cholesterol, triglycerides decreased not obvious. Conclusion Inflammation enhances the expression of LDL receptor on the cell membrane by promoting the expression of SREBP2 and SCAP in hepatocytes, leading to the deposition of cholesterol in liver cells.