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稳心颗粒通过调节钙/钙调蛋白依赖性激酶II信号通路对心肌肥厚和心律失常的影响

Effects of Wenxin Keli on Cardiac Hypertrophy and Arrhythmia via Regulation of the Calcium/Calmodulin Dependent Kinase II Signaling Pathway.

作者信息

Yang Xinyu, Chen Yu, Li Yanda, Ren Xiaomeng, Xing Yanwei, Shang Hongcai

机构信息

The Key Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.

Guang'anmen Hospital, Chinese Academy of Chinese Medical Sciences, Beijing 100053, China.

出版信息

Biomed Res Int. 2017;2017:1569235. doi: 10.1155/2017/1569235. Epub 2017 May 9.

DOI:10.1155/2017/1569235
PMID:28573136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5440795/
Abstract

We investigated the effects of Wenxin Keli (WXKL) on the Calcium/Calmodulin dependent kinase II (CaMK II) signal transduction pathway with transverse aortic constriction (TAC) rats. Echocardiographic measurements were obtained 3 and 9 weeks after the surgery. Meanwhile, the action potentials (APDs) were recorded using the whole-cell patch clamp technique, and western blotting was used to assess components of the CaMK II signal transduction pathway. At both 3 and 9 weeks after treatment, the fractional shortening (FS%) increased in the WXKL group compared with the TAC group. The APD of the TAC group was longer than that of the Sham group and was markedly shortened by WXKL treatment. Western blotting results showed that the protein expressions of CaMK II, phospholamban (PLB), and ryanodine receptor 2 (RYR2) were not statistically significant among the different groups at both treatment time points. However, WXKL treatment decreased the protein level and phosphorylation of CaMK II (Thr-286) and increased the protein level and phosphorylation of PLB (Thr-17) and the phosphorylation of RYR2 (Ser-2814). WXKL also decreased the accumulation of type III collagen fibers. In conclusion, WXKL may improve cardiac function and inhibit the arrhythmia by regulating the CaMK II signal transduction pathway.

摘要

我们用主动脉缩窄（TAC）大鼠研究了稳心颗粒（WXKL）对钙/钙调蛋白依赖性激酶II（CaMK II）信号转导通路的影响。术后3周和9周进行超声心动图测量。同时，采用全细胞膜片钳技术记录动作电位（APD），并用蛋白质印迹法评估CaMK II信号转导通路的组成成分。治疗后3周和9周时，与TAC组相比，WXKL组的左室短轴缩短率（FS%）均增加。TAC组的APD长于假手术组，而WXKL治疗可使其明显缩短。蛋白质印迹结果显示，在两个治疗时间点，不同组间CaMK II、受磷蛋白（PLB）和兰尼碱受体2（RYR2）的蛋白表达无统计学差异。然而，WXKL治疗降低了CaMK II（苏氨酸-286）的蛋白水平和磷酸化水平，增加了PLB（苏氨酸-17）的蛋白水平和磷酸化水平以及RYR2（丝氨酸-2814）的磷酸化水平。WXKL还减少了III型胶原纤维的蓄积。总之，WXKL可能通过调节CaMK II信号转导通路改善心脏功能并抑制心律失常。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/1d52212b1274/BMRI2017-1569235.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/275612141060/BMRI2017-1569235.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/1b08c9b2a106/BMRI2017-1569235.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/4d5a3074085c/BMRI2017-1569235.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/15cb4bc4b1bd/BMRI2017-1569235.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/0a8ca339101d/BMRI2017-1569235.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/1f3385e04488/BMRI2017-1569235.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/1d52212b1274/BMRI2017-1569235.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/275612141060/BMRI2017-1569235.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/1b08c9b2a106/BMRI2017-1569235.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/4d5a3074085c/BMRI2017-1569235.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/15cb4bc4b1bd/BMRI2017-1569235.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/0a8ca339101d/BMRI2017-1569235.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/1f3385e04488/BMRI2017-1569235.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8377/5440795/1d52212b1274/BMRI2017-1569235.007.jpg

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