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背景肝X受体是一种核受体,与细胞内胆固醇及糖等能量代谢有关。目的探讨肝X受体激动剂在体外对血管紧张素Ⅱ(Ang Ⅱ)诱导的肥大HL-1心肌细胞的作用。方法用Ang Ⅱ刺激诱导建立肥大心肌细胞模型,模型中加入肝X受体激动剂T0901317(1μmol/L) ,采用免疫荧光技术进行细胞染色,NI H图像J处理软件分析细胞表面积,3H亮氨酸掺入检测心肌细胞蛋白合成速率,定量实时PCR(realti me-PCR)法检测心房利钠肽(ANP) mRNA的表达水平。结果 Ang Ⅱ诱导HL-1心肌细胞肥大,表现为相对细胞面积的扩大(对照组1.00±0.16比Ang Ⅱ组2.00±0.21) ,ANP mRNA表达(对照组1.00±0.02比Ang Ⅱ组1.58±0.27)和3H亮氨酸掺入与对照组的比值的增加(对照组1.00±0.03比Ang Ⅱ组1.44±0.07 ,均P<0.05) ,肝X受体激动剂T0901317处理后能明显抑制以上改变( Ang Ⅱ组与T0901317 +Ang Ⅱ组比较,细胞面积:2.00±0.21比1.30±0.15 ;ANP mRNA表达:1.58±0.27比0.99±0.14 ;3H亮氨酸掺入:1.44±0.07比1.08±0.05 ,均P<0.05)。结论体外细胞试验,肝X受体激动剂T0901317可抑制HL-1心肌细胞的肥大。
Background Liver X receptors are nuclear receptors involved in the energy metabolism of cholesterol and sugar in cells. Objective To investigate the effect of liver X receptor agonist on hypertrophic HL-1 cardiomyocytes induced by angiotensin Ⅱ (Ang Ⅱ) in vitro. Methods The hypertrophic cardiomyocytes were induced by Ang Ⅱ stimulation. Liver X receptor agonist T0901317 (1μmol / L) was added into the model. The cells were stained with immunofluorescence technique. NIH image J software was used to analyze the cell surface area, 3H-leucine The protein synthesis rate of cardiomyocytes was detected by radioimmunoassay, and the mRNA expression of atrial natriuretic peptide (ANP) was detected by real-time PCR. Results Ang Ⅱ induced HL-1 cardiomyocyte hypertrophy with an increase of relative cell area (1.00 ± 0.16 in control group vs. 2.00 ± 0.21 in Ang Ⅱ group), ANP mRNA expression (1.00 ± 0.02 in control group vs 1.58 ± 0.27 in Ang Ⅱ group) And 3H-leucine (control group 1.00 ± 0.03 vs Ang Ⅱ group 1.44 ± 0.07, both P <0.05). The treatment with liver X receptor agonist T0901317 significantly inhibited the above changes Compared with T0901317 + Ang Ⅱ group, the cell area in group Ⅱ was 2.00 ± 0.21 than 1.30 ± 0.15, ANP mRNA expression was 1.58 ± 0.27 and 0.99 ± 0.14, and 3H and leucine incorporation was 1.44 ± 0.07 and 1.08 ± 0.05, both P <0.05). Conclusion In vitro cell experiments, liver X receptor agonist T0901317 can inhibit HL-1 cardiomyocyte hypertrophy.