AI Article Synopsis
- Apoptosis is crucial in the development of ischemic strokes, and studying it in models of brain injury shows promising insights.
- The study investigates the role of the Gadd45b protein in brain ischemia using adult male rats, where its expression was reduced using RNA interference.
- The results revealed that reducing Gadd45b led to larger brain injury areas, worse neurological outcomes, and increased neuronal apoptosis, suggesting Gadd45b helps protect against cell death in ischemic conditions.
Article Abstract
Apoptosis plays an essential role in ischemic stroke pathogenesis. Research on the process of neuronal apoptosis in models of ischemic brain injury seems promising. The role of growth arrest and DNA-damage-inducible protein 45 beta (Gadd45b) in brain ischemia has not been fully examined to date. This study aims to investigate the function of Gadd45b in ischemia-induced apoptosis. Adult male Sprague-Dawley rats were subjected to brain ischemia by middle cerebral artery occlusion (MCAO). RNA interference (RNAi) system, which is mediated by a lentiviral vector (LV), was stereotaxically injected into the ipsilateral lateral ventricle to knockdown Gadd45b expression. Neurologic scores and infarct volumes were assessed 24 h after reperfusion. Apoptosis-related molecules were studied using immunohistochemistry and Western blot analysis. We found that Gadd45b-RNAi significantly increased infarct volumes and worsened the outcome of transient focal cerebral ischemia. Gadd45b-RNAi also significantly increased neuronal apoptosis as indicated by increased levels of Bax and active caspase-3, and decreased levels of Bcl-2. These results indicate that Gadd45b is a beneficial mediator of neuronal apoptosis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4323375 | PMC |
| http://dx.doi.org/10.7150/ijbs.9813 | DOI Listing |
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