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Objective:To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury.Methods:The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg/mL, 3.0 mg/mL, 5.0 mg/mL) for 24 h,then cells were cultured in ischemia environment for 24 h and reperfusion environment for 1 h. The MTT and flow cytometry were used to detect the proliferation and apoptosis of human cardiac myocytes, respectively. The mRNA and protein expressions of Bcl-2 and Bax were measured by qRT-PCR and western blot, respectively.Results:Compared to the negative group, pretreated by tocilizumab could significantly enhance the proliferation viability and suppress apoptosis of human cardiac myocytes after suffering ischemia reperfusion injury(P<0.05).The expression of Bcl-2 in tocilizumab treated group were higher thanNC group(P<0.05), while theBax expression were lower(P<0.05).Conclusions:Tocilizumab could significantly inhibit apoptosis and keep the proliferation viability of human cardiac myocytes after suffering ischemia reperfusion injury. Tocilizumab may obtain a widely application in the protection of ischemia reperfusion injury.
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Objective_To explore the effect and the mechanism of isoflurane on human cardiac myocytes ( HCM) injury induced by anoxia/reoxygenation ( AR) .Methods_HCM cells were divided into control group ( con) , an-oxia/reoxygenation group (AR) and isoflurane (0.5%, 1%, 1.5%and 2%) treatment group (n=6).Cell via-bility, LDH activity, apoptosis and the expression level of Anoxia inducible factor-1α( HIF-1α) were detected using CCK-8 assay, LDH activity assay kit, Annexin V-FITC/PI staining, PCR and western blot, respectively. Results_Compared with the con group, cell viability decreased, LDH activity and apoptosis cells increased in AR group.Isoflurane can significantly relieve the decrease of cell viability, the increase of LDH activity and apoptosis cells, and the down-regulation of the mRNA and protein expression level of HIF-1αinduced by AR ( P<0.05 ) . Compared with AR group, the mRNA and protein expression level of HIF-1αin siRNA transfected group signifi-cantly decreased (P<0.05).2%isoflurane significantly relieve the increase of cell viability, the decrease of LDH activity and apoptotic cells induced by HIF-siRNA in AR injuried HCM cells(P<0.05).Conclusions_Isoflurane can protect HCM cells from AR injury partly through up-regulate the expression of HIF-1α.
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OBJECTIVE@#To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury.@*METHODS@#The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg/mL, 3.0 mg/mL, 5.0 mg/mL) for 24 h, then cells were cultured in ischemia environment for 24 h and reperfusion environment for 1 h. The MTT and flow cytometry were used to detect the proliferation and apoptosis of human cardiac myocytes, respectively. The mRNA and protein expressions of Bcl-2 and Bax were measured by qRT-PCR and western blot, respectively.@*RESULTS@#Compared to the negative group, pretreated by tocilizumab could significantly enhance the proliferation viability and suppress apoptosis of human cardiac myocytes after suffering ischemia reperfusion injury (P<0.05). The expression of Bcl-2 in tocilizumab treated group were higher than NC group (P<0.05), while the Bax expression were lower (P<0.05).@*CONCLUSIONS@#Tocilizumab could significantly inhibit apoptosis and keep the proliferation viability of human cardiac myocytes after suffering ischemia reperfusion injury. Tocilizumab may obtain a widely application in the protection of ischemia reperfusion injury.
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Objective: To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury. Methods: The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg/mL, 3.0 mg/mL, 5.0 mg/mL) for 24 h, then cells were cultured in ischemia environment for 24 h and reperfusion environment for 1 h. The MTT and flow cytometry were used to detect the proliferation and apoptosis of human cardiac myocytes, respectively. The mRNA and protein expressions of Bcl-2 and Bax were measured by qRT-PCR and western blot, respectively. Results: Compared to the negative group, pretreated by tocilizumab could significantly enhance the proliferation viability and suppress apoptosis of human cardiac myocytes after suffering ischemia reperfusion injury (. P<0.05). The expression of Bcl-2 in tocilizumab treated group were higher than NC group (. P<0.05), while the Bax expression were lower (. P<0.05). Conclusions: Tocilizumab could significantly inhibit apoptosis and keep the proliferation viability of human cardiac myocytes after suffering ischemia reperfusion injury. Tocilizumab may obtain a widely application in the protection of ischemia reperfusion injury.