Wenchao Yin, Haibin Jia, Wenzhi Wu, Lan Zhang, Chunyan Wang
{"title":"Effect of propofol on H2O2-induced necroptosis in rat cardiomyocytes","authors":"Wenchao Yin, Haibin Jia, Wenzhi Wu, Lan Zhang, Chunyan Wang","doi":"10.3760/CMA.J.ISSN.0254-1416.2019.11.026","DOIUrl":null,"url":null,"abstract":"Objective \nTo evaluate the effect of propofol on H2O2-induced necroptosis in rat cardiomyocytes. \n \n \nMethods \nH9C2 cells at the logarithmic growth phase were divided into 4 groups (n= 9 each) using a random number table method: control group (group C), H2O2 group, propofol group (group P) and dimethyl sulfoxide group (group D). Cells were incubated in normal DMEM medium in group C. H2O2 was added to the culture medium with the final concentration of 500 μmol/L in group H2O2.Propofol at the final concentration of 50 μmol/L and the equal volume of dimethyl sulfoxide were added to the cell medium at 30 min before H2O2 exposure in group P and group D, respectively.After 12-h culture or incubation with H2O2, cardiomyocytes necrosis was detected by PI staining, reactive oxygen species (ROS) level was determined by DCFH-DA staining, and the expression of receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL) was determined by Western blot. \n \n \nResults \nCompared with group C, necrosis rate and ROS level were significantly increased, and the expression of RIPK1, RIPK3 and MLKL was up-regulated in H2O2 and D groups (P<0.05). Compared with group H2O2, necrosis rate and ROS level were significantly decreased, and the expression of RIPK1, RIPK3 and MLKL was down-regulated in group P (P<0.05). \n \n \nConclusion \nPropofol can attenuate H2O2-induced necroptosis in cardiomyocytes of rats. \n \n \nKey words: \nPropofol; Hydrogen peroxide; Myocytes, cardiac; Necroptosis","PeriodicalId":10053,"journal":{"name":"中华麻醉学杂志","volume":"39 1","pages":"1376-1378"},"PeriodicalIF":0.0000,"publicationDate":"2019-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"中华麻醉学杂志","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3760/CMA.J.ISSN.0254-1416.2019.11.026","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Objective
To evaluate the effect of propofol on H2O2-induced necroptosis in rat cardiomyocytes.
Methods
H9C2 cells at the logarithmic growth phase were divided into 4 groups (n= 9 each) using a random number table method: control group (group C), H2O2 group, propofol group (group P) and dimethyl sulfoxide group (group D). Cells were incubated in normal DMEM medium in group C. H2O2 was added to the culture medium with the final concentration of 500 μmol/L in group H2O2.Propofol at the final concentration of 50 μmol/L and the equal volume of dimethyl sulfoxide were added to the cell medium at 30 min before H2O2 exposure in group P and group D, respectively.After 12-h culture or incubation with H2O2, cardiomyocytes necrosis was detected by PI staining, reactive oxygen species (ROS) level was determined by DCFH-DA staining, and the expression of receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL) was determined by Western blot.
Results
Compared with group C, necrosis rate and ROS level were significantly increased, and the expression of RIPK1, RIPK3 and MLKL was up-regulated in H2O2 and D groups (P<0.05). Compared with group H2O2, necrosis rate and ROS level were significantly decreased, and the expression of RIPK1, RIPK3 and MLKL was down-regulated in group P (P<0.05).
Conclusion
Propofol can attenuate H2O2-induced necroptosis in cardiomyocytes of rats.
Key words:
Propofol; Hydrogen peroxide; Myocytes, cardiac; Necroptosis