Abstract

To analyze the mechanism of dexmedetomidine through mitochondrial and endoplasmic reticulum oxidative stress pathway in neonatal rat cardiomyocytes is the main objective of the study. Sprague Dawley neonatal rats were selected as the research object and then control group (group A), hydrogen peroxide group (group B), dexmedetomidine group (Group C) and dexmedetomidine+hydrogen peroxide group were constructed (Group D), four groups of neonatal rat cardiomyocyte oxidative injury models. After drug treatment, the morphology, lactate dehydrogenase, reduced glutathione, reactive oxygen species, caspase-3, 8, 9 and 12 activities of neonatal rat cardiomyocytes were detected in turn. The mitochondrial membrane potential and apoptosis rate were detected by flow cytometry and glucose-regulated protein 78 and inositol-requiring enzyme 1 alpha were detected by Western blot, expression of B-cell lymphoma 2 and Bcl-2-associated X proteins. 500 μmol/l was selected as the best reaction concentration of hydrogen peroxide. Compared with group A, the activity levels of lactate dehydrogenase and reactive oxygen species in cardiomyocytes in group B increased significantly and the activity level of reduced glutathione decreased significantly. Compared with group B, the activity of reduced glutathione in group D was significantly increased, while the activity of lactate dehydrogenase and reactive oxygen species decreased significantly. The apoptosis rate of cardiomyocytes in group A was 18.36 %±5.68 % and that in group D was 39.64 %±9.36 %. Compared with group A, the apoptosis rate in group B increased significantly; there was no significant change in the apoptosis rate in group C. Compared with group A, glucose-regulated protein 78 and inositol-requiring enzyme 1 alpha significantly improved; compared with group B, GRP78 and IRE1α in group D significantly reduced. Dexmedetomidine can inhibit the oxidative stress response and apoptosis induced by hydrogen peroxide in neonatal rat cardiomyocytes.