Protective effect of TSA on PC12 cell injury induced by the deprivation of oxygen/glucose
JI Yu-hua
Abstract
JI Yu-hua
Abstract
Aim To study the protective effects of histone deacetylase inhibitor(HDACi),trichostatin A(TSA),on oxygen/glucose deprivation(OGD) injuried PC12 cells and its underlying mechanism.Methods PC12 OGD injury model was established by using cobalt chloride(CoCl2) and glucose-free medium,and treated by 1-640 nmol·L-1 TSA.Cell viability was measured by MTT assay,cell apoptosis and necrosis was observed by PI and Hoechst staining,and flow cytometry detection and fluorescence microscope were applied to determine the reactive oxygen species in each group.Results Compared with control group,80 nmol·L-1 TSA significantly improved cell viability and reduced intracellular reactive oxygen species(ROS).Conclusions TSA protects the OGD injured PC12 cells.The possible underlying mechanisms may be related to maintaining or increasing the acetylation level of the energy metabolism enzymes,whereby keeping the PC12 cells from the injury induced by OGD.
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Aim To study the protective effects of histone deacetylase inhibitor(HDACi),trichostatin A(TSA),on oxygen/glucose deprivation(OGD) injuried PC12 cells and its underlying mechanism.Methods PC12 OGD injury model was established by using cobalt chloride(CoCl2) and glucose-free medium,and treated by 1-640 nmol·L-1 TSA.Cell viability was measured by MTT assay,cell apoptosis and necrosis was observed by PI and Hoechst staining,and flow cytometry detection and fluorescence microscope were applied to determine the reactive oxygen species in each group.Results Compared with control group,80 nmol·L-1 TSA significantly improved cell viability and reduced intracellular reactive oxygen species(ROS).Conclusions TSA protects the OGD injured PC12 cells.The possible underlying mechanisms may be related to maintaining or increasing the acetylation level of the energy metabolism enzymes,whereby keeping the PC12 cells from the injury induced by OGD.
Key concepts: Trichostatin A, Viability assay, Reactive oxygen species, Apoptosis, Flow cytometry, Chemistry, Intracellular, MTT assay