丹参对高血压肥大心肌细胞中黏着斑激酶表达的影响

Influence of salvia miltiorrhiza on expression of focal adhesion kinase in cardiac myocytes of hypertrophic ventricle

目的分析丹参对高血压肥大心肌细胞中黏着斑激酶(FAK)表达的影响,探讨丹参抑制心肌肥大的可能机制.方法通过免疫荧光标记、共聚焦显微镜及Western blot等方法,检测WKY(WKY组)、自发性高血压大鼠(SHHR-A组)、丹参干预组(SHHR-B)和卡托普利干预组(SHHR-C)心肌细胞中FAK的表达及其分布.结果与WKY大鼠相比,FAK在心肌细胞中总蛋白、细胞膜蛋白、细胞核蛋白表达明显增加(均P< 0.01),而细胞质蛋白变化无统计学意义(P>0.05).SHHR-B组与SHHR-A组相比,FAK在SHHR-B大鼠中总蛋白、细胞膜蛋白、细胞核蛋白的表达均减少(均P<0.01),而细胞质蛋白保持不变(P>0.05).共聚焦显微镜观察发现FAK在SHHR大鼠细胞膜聚集明显,而丹参能减少FAK在细胞膜和细胞核的分布.结论丹参能抑制FAK在心肌细胞中总蛋白、细胞膜蛋白、细胞核蛋白的表达,减少FAK在细胞膜、细胞核中聚集,抑制心肌肥厚.

Objective To analyze the influence of salvia miltiorrhiza on the expression of focal adhesion kinase (FAK) in cardiac myocytes of hypertrophic ventricle,and to explore the mechanism of salvia niltiorrhiza in the inhibition of cardiac hypertrophy.Methods Spontaneously hypertensive rats (SHHR) were used as research objects.The expression and distribution of FAK in left ventricular myocardial cells were detected by immunofluorescent labeling,confocal microscopy,and Western blotting,and were compared among the salvia miltiorrhiza intervention group (SHHR-B),the captopril intervention group (SHHR-C),and the control rats (SHHR-A).Results Compared with the WKY rats,the expression of FAK was significantly increased in total protein,cytomembrane protein,and cyteblast protein (all P < 0.01),but not in cytoplasm protein (P > 0.05).Compared with that in the SHHR-A group,the expression of FAK in SHHR-B rats was decreased in total protein,cytomembrane protein,and cyteblast protein,P < 0.01),but that in cytoplasm protein remained unchanged (P > 0.05) in the SHHR-B group.Confocal microscopy showed that FAK accumulated significantly in the cytomembrane of the SHHR rats,and salvia miltiorrhiza could reduce the distribution of FAK in cytomembrane and cyteblast.Conclusions Salvia miltiorrhiza can inhibit the expression of FAK in total protein,cytomembrane protein,and cyteblast protein of cardiomyocytes,reduce the accumulation of FAK in cell membrane and cyteblast,and inhibit myocardial hypertrophy.