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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Zhang, Liyuan Li, Kun Sun, Rui Zhang, Yuan Ji, JianFeng Huang, Peigeng Yang, Hongying Tian, Ye |
| Abstract | Background It has been long recognized that cranial irradiation used for the treatment of primary and metastatic brain tumor often causes neurological side-effects such as intellectual impairment, memory loss and dementia, especially in children patients. Our previous study has demonstrated that whole-brain irradiation (WBI) can cause cognitive decline in rats. Minocycline is an antibiotic that has shown neuroprotective properties in a variety of experimental models of neurological diseases. However, whether minocycline can ameliorate cognitive impairment induced by ionizing radiation (IR) has not been tested. Thus this study aimed to demonstrate the potential implication of minocycline in the treatment of WBI-induced cognitive deficits by using a rat model. Methods Sprague Dawley rats were cranial irradiated with electron beams delivered by a linear accelerator with a single dose of 20 Gy. Minocycline was administered via oral gavages directly into the stomach before and after irradiation. The open field test was used to assess the anxiety level of rats. The Morris water maze (MWM) was used to assess the spatial learning and memory of rats. The level of apoptosis in hippocampal neurons was measured using immunohistochemistry for caspase-3 and relative markers for mature neurons (NeuN) or for newborn neurons (Doublecortin (DCX)). Neurogenesis was determined by BrdU incorporation method. Results Neither WBI nor minocycline affected the locomotor activity and anxiety level of rats. However, compared with the sham-irradiated controls, WBI caused a significant loss of learning and memory manifest as longer latency to reach the hidden platform in the MWM task. Minocycline intervention significantly improved the memory retention of irradiated rats. Although minocycline did not rescue neurogenesis deficit caused by WBI 2 months post-IR, it did significantly decreased WBI-induced apoptosis in the DCX positive neurons, thereby resulting in less newborn neuron depletion 12 h after irradiation. Conclusions Minocycline significantly inhibits WBI-induced neuron apoptosis, leading to less newborn neurons loss shortly after irradiation. In the long run, minocycline improves the cognitive performance of rats post WBI. The results indicate a potential clinical implication of minocycline as an effective adjunct in radiotherapy for brain tumor patients. |
| Related Links | https://ro-journal.biomedcentral.com/counter/pdf/10.1186/s13014-014-0281-8.pdf |
| Ending Page | 10 |
| Page Count | 10 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| DOI | 10.1186/s13014-014-0281-8 |
| Journal | Radiation Oncology |
| Issue Number | 1 |
| Volume Number | 9 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2014-12-12 |
| Access Restriction | Open |
| Subject Keyword | Cancer Research Oncology Radiotherapy Imaging Radiology Whole-brain irradiation Cognitive deficit Minocycline Newborn neuron Apoptosis Neurogenesis |
| Content Type | Text |
| Resource Type | Article |
| Subject | Radiology, Nuclear Medicine and Imaging Oncology |
| Journal Impact Factor | 3.3/2023 |
| 5-Year Journal Impact Factor | 3.6/2023 |
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