压力超负荷对大鼠左室心肌牵张敏感性钾通道TREK-1 mRNA和蛋白表达的影响

Changes of expression of stretch-activated potassium channel TREK-1 mRNA and protein induced by chronic pressure overload in rat left ventricle.

目的探讨压力超负荷状态下左室心肌牵张敏感性钾通道TREK-1mRNA及其蛋白表达的变化。方法雄性W istar大鼠被随机分为腹主动脉缩窄组(n=30)和假手术组。腹主动脉缩窄组依观察时间随机分为2,4,8周组各10只。每组观察期结束后,计算左右室肥厚指数(LVM I、RVM I)。HE染色观察压力超负荷对心肌组织结构的影响。采用RT-PCR和免疫组织化学SABC法分别检测牵张敏感性钾通道TREK-1mRNA与蛋白水平表达的改变。结果腹主动脉缩窄术后2周,出现左室肥厚,但无统计学意义。腹主动脉缩窄术后4,8周,左室肥厚指数较正常组明显增加(P<0.05),光镜下显示心肌肥厚。术后2,4,8周组左室心肌牵张敏感性钾通道TREK-1mRNA上调(P<0.05),心肌细胞内TREK-1蛋白表达明显增加(P<0.05)。结论压力超负荷致大鼠左室肥厚的同时可诱导牵张敏感性钾通道TREK-1的表达增加。

Objective To investigate expression changes of stretch-activated potassium channel TREK-1 mRNA and protein induced by coarctation of abdominal aorta （CAA）. Methods Male Wistar rats were randomly divided into four groups：CAA2w ,CAA4w,CAA8w, and sham-operated group（n = 10 in each group）. Left and right ventricular mass index （LVMI,RVMI） ,cardiac morphological changes were investigated in different groups. The expression of TREK-1 mRNA was examined by semi-quantitative RT-PCR, and the expression of TREK-1 protein was detected by immunohistochemistry. Results Compared to sham-operated group,left ventricles became hypertrophy at 2 weeks after coarctation of abdominal aorta,but it had no statistical significance;Left ventricular mass indes（LVMI） increased significantly at 4 and 8 weeks after abdominal coarctation（P〈0.05）, and hypertrophic cardiomyocytes were seen, under optioal microscope. TREK-1 mRNA strongly expressed and protein up-regulated in groups CAA2w, CAA4w and CAA8w （ P 〈0. 05）. Conclusions Expression of TREK-1 up-regulated during the progression of left ventricular hypertrophy induced by chronic pressure overload.