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Abstract

Protective Effect and Mechanism of Dexmedetomidine Pretreatment Mediated AMPK Pathway on Hypoxic Reoxygenation Injury in Rat Cardiomyocytes

Author(s): Qingrui Chen, Yingying Lin, Yulin Liu, Guoshao Zhu, Wenji Xie and Yingle Chen*
Department of Clinical Anesthesiology, The Affiliated Quanzhou First Hospital of Fujian Medical University, Quanzhou, Fujian Province 362002, 1Graduate School, Fujian Medical University, Fujian, Fuzhou, Fujian Province 350122, 2Department of Clinical Anesthesiology, Yongchun County Hospital, Quanzhou, Fujian Province 362000, China

Correspondence Address:
Yingle Chen, Department of Clinical Anesthesiology, The Affiliated Quanzhou First Hospital of Fujian Medical University, Quanzhou, Fujian Province 362002, E-mail: lsy13850@163.com


To examine the effect and mechanism of dexmedetomidine pretreatment mediated adenylate adenosine monophosphate-activated protein kinase pathway on hypoxic reoxygenation injured rat cardiomyocytes. A total of sixty Sprague-Dawley rats were allocated into three groups, namely the sham surgery group, model group, and dexmedetomidine intervention group, utilizing a random number table. Each group consisted of twenty rats. The model group and the intervention group of dexmedetomidine were used to prepare a rat myocardial hypoxia reoxygenation injury model using an improved thread occlusion method. The sham surgery group only underwent thoracotomy without ligation, and the intervention group of dexmedetomidine was pretreated with dexmedetomidine before establishing the model. Western blot was used to detect adenosine monophosphate-activated protein kinase, uncoupling protein 2, and Kruppel-like factor 2 proteins; using flow cytometry to detect the average fluorescence intensity of reactive oxygen species; detection of cell apoptosis rate using terminal deoxynucleotidyl transferase dUTP nick end labeling method; using the enzyme-linked immunosorbent assay detection kit manual to detect serum interleukin-6 and tumor necrosis factor-alpha, interleukin-1 beta and the levels of various indicators such as superoxide dismutase and malondialdehyde. Adenosine monophosphate-activated protein kinase, Kruppel-like factor 2, and uncoupling protein 2 proteins in the myocardium of the model group rats were markedly lower than those of the sham operation group; adenosine monophosphate-activated protein kinase, Kruppel-like factor 2, and uncoupling protein 2 in the myocardium of rats in the dexmedetomidine intervention group were markedly higher than the model group. The superoxide dismutase level of the model group rats was markedly reduced than the sham operation group, with malondialdehyde, interleukin-6 and tumor necrosis factor-alpha, interleukin-1 beta was markedly higher than that of the sham surgery group; superoxide dismutase, malondialdehyde, interleukin-6 and tumor necrosis factor-alpha in the intervention group of dexmedetomidine were markedly higher than the model group, tumor necrosis factor-alpha, interleukin-1 beta was markedly reduced than that of the model group. Dexmedetomidine can activate adenosine monophosphate-activated protein kinase pathway, upregulation of uncoupling protein 2 expressions and the inhibition of mitochondrial reactive oxygen species production are observed, thereby restraining the oxidative irritability of myocardial tissue under hypoxia/reoxygenation conditions and playing a role in myocardial cytoprotection.

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Citations : 61564

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