脾气虚大鼠心肌细胞线粒体Lon蛋白酶和ClpXP复合物表达的研究  

Expression of Lon protease and ClpXP complex in mitochondria of rat cardiomyocytes with spleen qi deficiency

作　　者：李振钰 许欣竹 刘文俊 王路[1] 于化新[1] 王凌志[1] 刘旭东[1] 刘慧慧[1] 单德红[1] LI Zhen-yu;XU Xin-zhu;LIU Wen-jun;WANG Lu;YU Hua-xin;WANG Ling-zhi;LIU Xu-dong;LIU Hui-hui;SHAN De-hong(Basic Medical College,Liaoning University of Traditional Chinese Medicine,Shenyang 110847,China;Liaoning Vocational College of Medicine,Shenyang 110101,China)

机构地区：[1]辽宁中医药大学基础医学院,沈阳110847 [2]辽宁医药职业学院,沈阳110101

出　　处：《中华中医药杂志》2021年第6期3616-3619,共4页China Journal of Traditional Chinese Medicine and Pharmacy

基　　金：国家自然科学基金项目(No.81673851)。

摘　　要：目的:通过研究心肌细胞线粒体L o n蛋白酶和C l p X P复合物的表达,围绕线粒体未折叠蛋白反应(UPRmt)探讨脾病及心的可能机制。方法:16只雄性SD大鼠随机分为正常组和脾气虚证模型组(模型组);鼠尾动脉无创测压法测定血压;心脏彩超检查心脏功能;透射电镜观察心肌细胞线粒体形态;ELISA法检测三磷酸腺苷(ATP)和MDA水平,Western Blot法检测心肌细胞线粒体Lon蛋白酶和ClpXP复合物的表达。结果:与正常组比较,模型组心率、收缩压、舒张压、左室射血分数和左室短轴缩短率均下降(P<0.01),线粒体内可见致密颗粒,ATP水平下降(P<0.01),MDA含量升高(P<0.01),Lon蛋白酶和ClpX表达均升高(P<0.05,P<0.01),但ClpP表达变化不明显。结论:脾病及心的现代医学机制可能与心肌细胞UPRmt未充分启动所导致的线粒体蛋白失稳态有关。Objective:To explore the possible mechanism of spleen disease affecting the heart based on the mitochondrial unfolded protein response(UPRmt),expressions of Lon protease and complex ClpXP was investigated.Methods:Sixteen male SD rats were randomly divided into the normal group and deficiency of spleen qi group(model group);non-invasive arterial blood pressure device was used to measure tail artery blood pressures.Doppler echocardiography was applied to detect the cardiac function;transmission electron microscopy was used to observe the mitochondrial morphology in myocardiac cells.ELISA was employed to test ATP and malondialdehyd(MDA)levels.Western Blot was utilized to check expressions of Lon protease and complex ClpXP.Results:Compared with those in the normal group,levels of heart rate,systolic pressue,diastolic pression,left ventricular ejection factor and fraction shortening were all reduced(P<0.01),dense particles appeared in mitochondria,the ATP level was reduced(P<0.01),the MDA level was increased(P<0.01),expressions of LonP and ClpX were increased(P<0.05,P<0.01),but the expression of ClpP was unaltered in the model group.Conclusion:The modern medical mechanism of spleen disease affecting the heart might be related to mitochondrial protein de-homeostasis caused by wearker UPRmt in myocardiac working cells.

关 键 词：脾气虚 脾病及心 线粒体未折叠蛋白反应 Lon蛋白酶 ClpXP复合物 

分 类 号：R-332[医药卫生] R256.3