Hydrogen sulfide protects PC12 cells against chemical hypoxia-induced injury by inhibing p38MAPK
Lan Ai-ping
Abstract
Lan Ai-ping
Abstract
Aim To investigate whether hydrogen sulfide(H 2 S) protected PC12 cells against chemical hypoxia-induced injury by inhibiting p38 MAPK.Methods PC12 cells were treated with cobalt chloride(CoCl 2 ) to set up a chemical hypoxia-induced cellular injury model.Cell viability was tested by cell counter kit(CCK-8) ;morphological changes of apoptotic cells were detected by Hochest 332580 staining;intracellular level of reactive oxygen species(ROS) was measured by DCFH-DA staining and photofluorograph;mitochondrial membrane potential(MMP) was observed by rhodamine 123(RH123) staining and photofluorography;the expression of p38MAPK was determined by Western blot assay.Results Exposure of PC12 cells to 600μmol· L -1 CoCl2 for 2 h significantly enhanced phosphorylated(p) p38MAPK expression.Pretreatment with 400 μmol·L -1 NaHS(a donor of H 2 S) for 30 min prior to exposure of PC12 cells to 600μmol·L -1 CoCl2 not only inhibited CoCl2 induced increase in expression of p38MAPK,but also protected PC12 cells against injuries induced by 600μmol·L -1 CoCl2,enhancing cell viability and decreasing amount of apoptotic cells and intracellular ROS level,as well as loss of MMP.Similarly,pretreatment with SB302580(20μmol·L-1) ,an inhibitor of p38MAPK,for 60 min prior to exposure of PC12 cells to CoCl2 also conferred the same cytoprotective effect of H2 S.Conclusions p38MAPK mediates CoCl2-induced injuries in PC12 cells.H2 S protects PC12 cells against chemical hypoxia-induced injury by inhibiting p38MAPK expression and oxidative stress.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Aim To investigate whether hydrogen sulfide(H 2 S) protected PC12 cells against chemical hypoxia-induced injury by inhibiting p38 MAPK.Methods PC12 cells were treated with cobalt chloride(CoCl 2 ) to set up a chemical hypoxia-induced cellular injury model.Cell viability was tested by cell counter kit(CCK-8) ;morphological changes of apoptotic cells were detected by Hochest 332580 staining;intracellular level of reactive oxygen species(ROS) was measured by DCFH-DA staining and photofluorograph;mitochondrial membrane potential(MMP) was observed by rhodamine 123(RH123) staining and photofluorography;the expression of p38MAPK was determined by Western blot assay.Results Exposure of PC12 cells to 600μmol· L -1 CoCl2 for 2 h significantly enhanced phosphorylated(p) p38MAPK expression.Pretreatment with 400 μmol·L -1 NaHS(a donor of H 2 S) for 30 min prior to exposure of PC12 cells to 600μmol·L -1 CoCl2 not only inhibited CoCl2 induced increase in expression of p38MAPK,but also protected PC12 cells against injuries induced by 600μmol·L -1 CoCl2,enhancing cell viability and decreasing amount of apoptotic cells and intracellular ROS level,as well as loss of MMP.Similarly,pretreatment with SB302580(20μmol·L-1) ,an inhibitor of p38MAPK,for 60 min prior to exposure of PC12 cells to CoCl2 also conferred the same cytoprotective effect of H2 S.Conclusions p38MAPK mediates CoCl2-induced injuries in PC12 cells.H2 S protects PC12 cells against chemical hypoxia-induced injury by inhibiting p38MAPK expression and oxidative stress.
Key concepts: Viability assay, Reactive oxygen species, Chemistry, Apoptosis, Molecular biology, Oxidative stress, Hypoxia (environmental), p38 mitogen-activated protein kinases