基于油酰乙醇胺的脂肪性肝炎新靶点机制及数据分析

发布时间：2018-03-04 13:24

本文选题：油酰乙醇胺(OEA)　切入点：脂肪性肝炎　出处：《中国老年学杂志》2015年15期 　论文类型：期刊论文

【摘要】：目的分析基于油酰乙醇胺(OEA)脂肪性肝炎新靶点机制及数据。方法造模Hep G2细胞,采用四甲基偶氮唑蓝(MTT)法检测细胞活力,结合油红染色及甘油三酯(TG)含量确认非酒精性脂肪肝(NAFLD)及脂肪性肝炎(NASH)体外模型建立;以OEA和阳性对照药物处理6、10、12 h,检测TG含量,采用定量聚合酶链式反应(PCR)检测脂代谢相关基因表达,并采用Western印迹法检测过氧化物酶体增殖激活受体(PPAR)α等。结果致NAFLD和NASH的最佳浓度为0.25 mmol/L油酸,细胞模型含0.25 mmol/L油酸组TG含量〔(5.516±0.262)mg/dl〕显著高于空白对照组〔(1.260±0.104)mg/dl〕(P0.05);各种浓度OEA模型的TG含量均显著低于空白对照组(P0.05);PCR结果显示,OEA浓度为50μmol/L时,可提高PPARα、去乙酰化酶(Sirt I)、肉碱棕榈酰转移酶(CPT)-I及脂蛋白脂肪酶(LPL)表达,降低固醇调节元件结合蛋白(SREBP)-1c、肿瘤坏死因子(TNF)α及乙酰辅酶A羧化酶(ACC)表达(P0.05)。结论 OEA可通过激活脂代谢基因PPARα、Sirt I、CPT-I、LPL的表达及抑制SREBP-1c、TNFα、ACC基因的表达,缓解NAFLD和NASH。
[Abstract]:Objective to analyze the new target mechanism and data of fatty hepatitis based on oleyl ethanolamine (OEA). Methods Hep G2 cells were modeled and the viability of the cells was detected by tetramethylazolazolium (MTT) assay. The in vitro model of nonalcoholic fatty liver (NAF LDD) and fatty hepatitis was established by oil red staining and triglyceride (TG) content, treated with OEA and positive control drugs for 12 h, TG content was detected. Quantitative polymerase chain reaction (PCR) was used to detect the expression of genes related to lipid metabolism, and Western blotting was used to detect the peroxisome proliferation-activated receptor (PPAR) 伪. Results the optimal concentration of NAFLD and NASH was 0.25 mmol/L oleic acid. The TG content in the cell model containing 0.25 mmol/L oleic acid was 5.516 卤0.262 mg / dl) significantly higher than that in the control group (1.260 卤0.104 渭 g / dlg / dll), and the TG content in all concentrations of OEA model was significantly lower than that in the blank control group (P0.05mg / dll) when the concentration of OEA was 50 渭 mol/L. It could increase the expression of PPAR 伪, deacetylase, carnitine palmitoyltransferase (PPAR) and lipoprotein lipase (LPL). The expression of steroid regulatory element binding protein (SREBP) -1c, tumor necrosis factor TNFa (TNFa) and acetyl coA carboxylase (OEA) was reduced by P0.05. Conclusion OEA can alleviate the expression of NAFLD and NASS by activating the expression of the lipid metabolism gene PPAR 伪 and inhibiting the expression of SREBP-1cTNF- 伪.
【作者单位】：福建医科大学附属第一医院干部科;
【分类号】：R575.5

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