Knockdown of TRIM32 Protects Hippocampal Neurons from Oxygen–Glucose Deprivation-Induced Injury
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Tripartite motif 32 (TRIM32) is a member of TRIM family that plays a potential role in neural regeneration. However, the biological function of TRIM32 in cerebral ischemia reperfusion injury has not been investigated. In the present study, we evaluated the expression level of TRIM32 in hippocampal neurons following oxygen–glucose deprivation/reperfusion (OGD/R). The results showed that TRIM32 expression was significantly elevated in hippocampal neurons subjected to OGD/R as compared to the neurons cultured in the normoxia condition. To further evaluate the role of TRIM32, hippocampal neurons were transfected with TRIM32 small interfering RNA (si-TRIM32) to knock down TRIM32. We found that knockdown of TRIM32 improved cell viability of OGD/R-stimulated hippocampal neurons. Generation of reactive oxygen species was decreased, while contents of superoxide dismutase and glutathione peroxidase were increased after si-TRIM32 transfection. Knockdown of TRIM32 suppressed cell apoptosis, as proved by the increased bcl-2 expression along with decreased bax expression and caspase-3 activity. We also found that TRIM32 knockdown enhanced OGD/R-induced activation of Nrf2 signaling pathway in hippocampal neurons. Furthermore, siRNA-Nrf2 was transfected to knock down Nrf2. SiRNA-Nrf2 transfection reversed the protective effects of TRIM32 knockdown on neurons. These data suggested that knockdown of TRIM32 protected hippocampal neurons from OGD/R-induced oxidative injury through activating Nrf2 signaling pathway.
KeywordsTripartite totif 32 (TRIM32) Cerebral ischemia reperfusion (I/R) injury Hippocampal neurons Oxygen–glucose deprivation/reperfusion (OGD/R) Oxidative stress Nrf2 signaling pathway
This work was supported by the National Natural Science Foundation of China (No. 81702955), the Scientific Research Program Funded by Department of Science and Technology of Shaanxi Province (Nos. 2018JM7066, 2018JM7065, 2018KJXX-34, 2019JZ-38), Scientific Research Program Funded by Shaanxi Provincial Education Department (Nos. G201711840002, G201711840006), the Leading Disciplines Development Government Foundation of Shaanxi Province (No.3-1001), grant from the Shannxi Key Laboratory of Ischemic Cardiovascular Disease (No. 2017ZDKF01), supporting Program Funded by Xi’an Medical University (Nos. 2018XNRC07, 2018GJFY02, 2017GJFY25, 2016PT06).
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Conflicts of interest
The authors have no competing interests to disclose.
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