PCBP2在压力负荷诱导的小鼠心肌肥厚发生中的作用

The effect of PCBP2 on the development of cardiac hypertrophy induced by pressure overloading in mice

目的 探讨PCBP2在压力负荷诱导的小鼠心肌肥厚发生过程中的作用.方法 选取8～10周龄的雄性C57BL/6小鼠20只,体重23～28 g,随机分为2组,每组各10只,分别施以主动脉缩窄术（TAC组）和假手术（Sham组）.术后4周应用超声心动图评价小鼠的心脏功能,应用心脏重量与体重之比（HW/BW）定量评价心肌肥厚程度.Real-time PCR检测心肌肥厚标志物Nppa、β-MHC （Myh7）的mRNA水平,同时检测PCBP2 mRNA水平.Western blot方法检测Nppa、β-MHC及PCBP2的蛋白水平.比较分析两组之间的差异.结果 与Sham组相比,TAC组小鼠的心肌肥厚程度明显增加[TAC组（8.23±1.88）mg/g比Sham组（4.89±0.68）mg/g],左心室射血分数[TAC组（41.38±2.22）％比Sham组（59.15±3.58）％]及短轴收缩率[TAC组（33.61±0.92）％比Sham组（43.87±1.37）％]明显降低（P＜0.05）.TAC组的心肌肥厚标志物Nppa、β-MHC的mRNA水平及蛋白水平均明显高于Sham组（P＜0.05）.然而,TAC组PCBP2mRNA水平及蛋白水平却明显低于Sham组（P＜0.05）,与心肌标志物Nppa、β-MHC的变化趋势相反.结论 PCBP2在压力负荷诱导的小鼠心肌肥厚发生过程中起着负性调节作用,上调PCBP2表达可能会抑制心肌肥厚的发展.

Objective The pressure overload cardiac hypertrophy was constructed by transaortic constriction（TAC ） in mice. To explore the effect of PCPB2 on the development of pressure overload cardiac hypertrophy in mice. Methods 20 male C57BL/6 mice （age 8-10 weeks, weight 23-28 kg） were used to construct the model. The mice were divided into 2 groups： TAC group（TAC surgery） and Sham group（Sham surgery）. Cardiac function was evaluated by echocardiography at postoperative 4 weeks. Also, the degree of cardiac hypertrophy was assessed with the ratio of heart weight/body weight （HW/BW）. Real-time PCR was used to detected the mRNA of PCBP2 and cardiac hypertrophic marker （Nppa,β-MHC）. Western blot was used to examined the protein of PCBP2 and cardiac hypertrophic markers （Nppa, β-MHC）. The differences between the two groups were analyzed. Results Compared with Sham group, cardiac hypertrophy and HW/BW ratio were significantly higher in TAC group[TAC group （8.23± 1.88 ）mg/g vs Sham group （4.89±0.68）mg/g ], but cardiac function was lower in TAC group [ LVEF ： TAC group （41.38±2.22）% vs Sham group （59.15±3.58）%; LVFS： TAC group （33.61±0.92）% vs Sham group （43.87±1.37）%（P〈0.05）]. The mRNA or proteins of Nppa and β-MHC of TAC group were higher than those of Sham group（P〈0.05）. However, both the mRNA and protein of PCBP2 were significantly lower than those of Sham group（P〈0.05）. Conclusion PCBP2 was a negative factor for the development of pressure overload cardiac hypertrophy in mice. Upregulation of PCBP2 may be able to inhibit the development of cardiac hypertrophy.