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目的探讨RNA结合蛋白QKI在血管紧张素Ⅱ诱导的心肌细胞肥大中的作用。方法将H9C2细胞分为对照组与心肌肥大组(AngⅡ组),AngⅡ组采用血管紧张素Ⅱ(10-7 mol/L)刺激H9C2细胞建立肥大模型;2组均采用转染小干扰RNA抑制QKI的表达,腺病毒感染H9C2细胞过表达QKI5和QKI6,应用Western blot检测H9C2细胞中QKI水平,应用实时定量RCR检测对照组及AngⅡ组作用6,12,18,24,36h时心房利钠多肽表达水平。结果与对照组比较,AngⅡ组作用12h总QKI增加,其中QKI6升高明显(P<0.05);AngⅡ+siQKI组心房利钠多肽水平较AngⅡ+NC组增加(P<0.05);AngⅡ+Ad-QKI5组心房利钠多肽水平与AngⅡ+Ad-Ctrl组比较差异无统计学意义(P>0.05),AngⅡ+Ad-QKI6组心房利钠多肽水平较AngⅡ+Ad-Ctrl组降低(P<0.05)。结论 QKI6可抑制心肌肥大。
Objective To investigate the role of RNA binding protein QKI in cardiomyocyte hypertrophy induced by angiotensin Ⅱ. Methods H9C2 cells were divided into control group and cardiac hypertrophy group (AngⅡ group). H9C2 cells were stimulated with angiotensinⅡ (10-7 mol / L) in Ang Ⅱ group to establish a hypertrophic model. Both groups were transfected with small interfering RNA to inhibit QKI The expression of QKI5 and QKI6 in H9C2 cells was overexpressed by adenovirus. The QKI level in H9C2 cells was detected by Western blot. Real-time quantitative RCR was used to detect the expression of atrial natriuretic peptide at 6, 12, 18, 24 and 36 h Level. Results Compared with the control group, the total QKI of AngⅡgroup increased at 12h, and the QKI6 increased significantly (P <0.05); Ang Ⅱ + siQKI group increased atrial natriuretic peptide level compared with AngⅡ + NC group (P <0.05) The level of atrial natriuretic peptide in QKI5 group was not significantly different from that in Ang Ⅱ + Ad-Ctrl group (P> 0.05). The atrial natriuretic peptide level in AngⅡ + Ad-QKI6 group was lower than that in AngⅡ + Ad-Ctrl group . Conclusion QKI6 can inhibit cardiac hypertrophy.