USP14 regulates H2O2 induced oxidative stress in H9c2 cells
10.3969/j.issn.1000-4718.2017.07.009
- VernacularTitle:去泛素化酶USP14调控H2O2诱导的H9c2细胞氧化应激损伤
- Author:
Hongjiao GU
;
Xiaohua CHEN
;
Tianyu KONG
;
Huan HU
;
Ningning LIU
;
Xuming XIONG
;
Zhenhui ZHANG
- Keywords:
Ubiquitin-specific protease 14;
IU1;
Oxidative stress;
Apoptosis;
Mitogen-activated protein kinase
- From:
Chinese Journal of Pathophysiology
2017;33(7):1209-1213
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To evaluate the effect of inhibiting ubiquitin-specific protease 14 (USPl4) activity on oxidative stress induced by H2O2 of H9c2 cells.METHODS: The H9c2 cells were incubated with H2O2 at 25 μmol/L for 2 h to establish the oxidative stress injury model.The cells were divided into control group, H2O2 group, IU1 group (25 μmol/L or 50 μmol/L) and IU1+ H2O2 group.The H9c2 cells activity was measured by MTS assay.The level of intracellular reactive oxygen species (ROS) and cell survival rate were analyzed by flow cytometry assay.The changes of the mitogen-activated protein kinase (MAPK) family related proteins were detected by Western blot.RESULTS: Compared with control group, the cell activity and the viability rate in H2O2 group were decreased (P<0.05), while the intracellular ROS, the protein levels of Bax/Bcl-2, P53, p-ERK1/2, p-JNK and p-P38 were increased (P<0.05).Compared with H2O2 group, the cell activity and the viability rate of the H9c2 cells in IU1+H2O2 group were increased (P<0.05), while the intracellular ROS, the protein levels of Bax/Bcl-2, P53, p-ERK1/2, p-JNK and p-P38 were decreased (P<0.05).CONCLUSION: Inhibition of USPl4 activity reduces the oxidative stress injury of the H9c2 cells.The mechanism may be related to inhibition of the MAPK signaling and down-regulation of apoptosis related proteins.
