Appearance of neural stem cells around the damaged area following traumatic brain injury in aged rats

Abstract

We have previously reported free radical production after traumatic brain injury (TBI), which induces neural stem cell (NSC) degeneration and death. However, the effects of aging on NSC proliferation around the damaged area following TBI have not been investigated. Therefore, in this study, we used 10-week (young group) and 24-month-old (aged group) rat TBI models to investigate the effects of aging on NSC proliferation around damaged tissue using immunohistochemical and ex vivo techniques. Young and aged rats received TBI. At 1, 3 and 7 days after TBI, immunohistochemical and lipid peroxidation studies were performed. Immunohistochemistry revealed that the number of nestin-positive cells around the damaged area after TBI in the aged group decreased significantly when compared with those in the young group (P < 0.01). However, the number of 8-hydroxy-2'-deoxyguanosine-, 4-hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells and the level of peroxidation around the damaged area after TBI significantly increased in the aged group, compared with those in the young group (P < 0.01). Furthermore, almost all ssDNA-positive cells in young and aged groups co-localized with NeuN and nestin staining. Ex vivo studies revealed that neurospheres, which differentiated into neurons and glia in culture, could only be isolated from injured brain tissue in young and aged groups at 3 days after TBI. These results indicate that, although there were fewer NSCs that have the potential to differentiate into neurons and glia, these NSCs escaped free radical-induced degeneration around the damaged area after TBI in the aged rat brain.

Exercise training for neural recovery in a restricted sample of pediatric brain tumor survivors: a controlled clinical trial with crossover of training versus no training

“…By harnessing these endogenous processes, exercise promotes brain recovery in rodent models of hypoxia, 35 radiation, 36 and traumatic brain injury. 37 Consistent with this, we found that increased fitness levels were significantly and marginally related to decreased RT and increased hippocampal volume, respectively.…”

Isosteviol sodium injection improves outcomes by modulating TLRs/NF-κB-dependent inflammatory responses following experimental traumatic brain injury in rats

“…Many studies reported that the pathological processes including inflammatory response, apoptosis, and loss of neurons usually reached the maximum peak at 3 days after TBI injury 29 – 34 . To further explore the mechanism underlying the STVNa-mediated neuroprotective effects, the levels of TLR2, TLR4, and NF-κB were measured after the administration of STVNa for 3 days following TBI (Fig.…”

Stem cell therapy for neurological disorders: A focus on aging

“…Levels of antioxidant enzymes such as catalase, glutathione, and superoxide dismutase are suppressed via post-transcriptional modification during normal aging in rat models (Itoh et al, 2013). Neural parenchyma has minute concentrations of antioxidant enzymes as compared to other tissue types, due to the resident NSC population dwindling with age (Itoh et al, 2013).…”

“…Levels of antioxidant enzymes such as catalase, glutathione, and superoxide dismutase are suppressed via post-transcriptional modification during normal aging in rat models (Itoh et al, 2013). Neural parenchyma has minute concentrations of antioxidant enzymes as compared to other tissue types, due to the resident NSC population dwindling with age (Itoh et al, 2013). Because TBI leads to the exacerbation of reactive oxygen species production, a more pronounced ebbing in the NSC population was seen following injury, indicating caspase-induced apoptosis (Itoh et al, 2013).…”