All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Abstract

Protective Effect and Mechanism of Dexmedetomidine on Myocardial Ischemia-Reperfusion Injury by Regulating Titin/Myosin Heavy Chain Signal Axis

Author(s): Mawen Lei*, Kang Luo, Y. Wang and K. Peng
Department of Anesthesiology, Chenzhou No.1 People's Hospital, Chenzhou, Hunan Province 423000, 1Department of Anesthesiology, The Third Affiliated Hospital, The University of South China, Hengyang, Hunan Province 421900, 2Department of Anesthesiology, Hunan Provincial People's Hospital, Changsha, Hunan Province 410005, 3Department of Cardiovascular Medicine, The First Affiliated Hospital, University of South China, Hengyang, Hunan Province 421000, China

Correspondence Address:
Mawen Lei, Department of Anesthesiology, Chenzhou No.1 People's Hospital, Chenzhou, Hunan Province 423000, China, E-mail: leimawen@163.com


To examine the protective impact of dexmedetomidine on myocardial ischemia-reperfusion injury, and to clarify the relationship between dexmedetomidine and titin/myosin heavy chain signal axis. Rat cardiac H9c2 cells were purchased as the research object. They were divided into three groups; blank control group, hypoxia concentration incubation group (hypoxia group) and dexmedetomidine group. The lactate dehydrogenase, cardiac troponin I and creatine kinase-myocardial band in myocardial cells of rats in hypoxia group were higher than the blank control group. The lactate dehydrogenase, cardiac troponin I and creatine kinase-myocardial band in myocardial cells of rats in differentially expressed gene were reduced than hypoxia group. Compared with the control group, in the hypoxia group, there was no discernible variation in the level of telomerase in cardiomyocytes. The telomerase level of cardiomyocytes in the differentially expressed gene was higher than the hypoxia group. Compared with the control group, the titin protein in myocardial cells of hypoxia group was decreased, the beta-myosin heavy chain protein was increased while the level of titin in cardiac myocytes of differentially expressed gene was higher than that of hypoxia group, and the beta-myosin heavy chain was reduced than hypoxia group. Compared with the blank control group, the phospho-extracellular signal regulated kinases protein in cardiac myocytes of rats in hypoxia group and differentially expressed gene was lower, and the nuclear factor kappa B protein was higher. However, the phospho-extracellular signal regulated kinases protein in cardiac myocytes of rats in differentially expressed gene was higher than in hypoxia group and the nuclear factor kappa B was reduced than hypoxia group. The phospho-phosphatidylinositol-3 kinase and phospho-protein kinase B in cardiac myocytes of rats in hypoxia group and differentially expressed gene were higher than the blank control group, and the phospho-phosphatidylinositol-3 kinase and phospho-protein kinase B in rats in differentially expressed gene were higher than hypoxia group. The protective effect of dexmedetomidine on myocardial ischemia-reperfusion injury may be related to reducing cardiomyocyte apoptosis and inhibiting titin differentially expressed gene radiation by activating extracellular signal regulated kinases 1/2 and phosphatidylinositol-3 kinase signaling pathways.

Full-Text | PDF

 
 
Google scholar citation report
Citations : 69022

Indian Journal of Pharmaceutical Sciences received 69022 citations as per google scholar report