IGF-1介导的钙调神经磷酸酶信号通路在心肌肥厚中的作用及人参皂苷Rb1的干预效应

Calcineurin signaling pathways induced by IGF -1 in myocardial hypertrophy of the functions and ginsenoside Rbl intervention effects

目的通过建立大鼠心肌肥厚模型观察人参皂苷Rb1对胰岛素样生长因子-1（IGF-1）介导的心肌肥厚的影响。方法采用手术缩窄腹主动脉的方法建立大鼠心肌肥厚模型。40只大鼠随机分为手术组（模型组、Rb1组、缬沙坦组，每组10只）及假手术组（10只）。4组大鼠分别给予相应处理，常规饲养6周后：测定颈动脉收缩压，计算左心室肥厚指数（LVMI），ELISA法测定大鼠血清IGF-1水平，Masson染色观察心肌组织变化，Westernblot法测定大鼠心肌组织钙调神经磷酸酶（CaN）的含量。结果与假手术组比较，手术组大鼠的颈动脉收缩压、LVMI、IGF-1及CaN均明显增高，差异有统计学意义（P〈0．05）；与模型组比较，Rb1组的颈动脉收缩压、LVMI、IGF-1及CaN均明显降低，差异有统计学意义（P〈0．05）。结论人参皂苷Rb1能有效抑制大鼠的心肌肥厚，其作用可能与降低IGF-1及其下游通路CaN的表达有关。

Objective Through the establishment of the rat myocardial hypertrophy model, to observe the inffluence of ginsenoside Rbl to myocardial hypertrophy induced by insulin - like growth factor - 1 （ IGF - 1 ）. Methods By the method of narrowing the abdominal aorta, the rat myocardial hypertrophy model establish was established. 40 rats were randomly divided into treatment group （model group, ginsenoside Rbl group, Valsartan group） and Sham group, and ev- ery group had 10 rats. 4 groups of rats were given corresponding drugs respectively. After six weeks of conventional feeding, determine the carotid artery systolic blood pressure, calculate left ventricular mass index（LVMI） , determine the ex- pression of IGF - 1 of the rat myocardial by ELISA method, observe the myocardial organization change by Masson dyeing, determine calcineurin （CaN） content of the rat myocardial by Western blot method. Results Compared with Sham group, the carotid artery systolic blood pressure, LVMI, IGF - 1 and CaN of treatment group were obviously increased, the difference was statistically significant （ P 〈 0.05 ） ; Compared with model group, the carotid artery systolic blood pres- sure, LVMI, IGF - 1 and CaN of downstream pathways of ginsenoside Rbl group were significantly lower, the difference was statistically significant （ P 〈 0.05 ）. Conclusion Ginsenoside Rbl can effectively restrain the rat myocardial hyper- trophy, in which the effects may be related to reducing the expression of IGF - 1, and then holding the calcineurin signa- ling pathways of downstream channel of the activation.