RESUMO
Repeated traumatic brain injury, leads to cumulative neuronal injury and neurological impairments. There are currently no effective treatments to prevent these consequences. Growing interest is building in the use of transcranial photobiomodulation (PBM) therapy to treat traumatic brain injury. Here, we examined PBM in a repeated closed head injury (rCHI) rat model. Rats were administered a total of three closed head injuries, with each injury separated by 5 days. PBM treatment was initiated 2 hours after the first injury and administered daily for a total of 15 days. We found that PBM-treated rCHI rats had a significant reduction in motor ability, anxiety and cognitive deficits compared to CHI group. PBM group showed an increase of synaptic proteins and surviving neurons, along with a reduction in reactive gliosis and neuronal injury. These findings highlight the complexity of gliosis and neuronal injury following rCHI and suggest that PBM may be a viable treatment option to mitigate these effects and their detrimental consequences.
Assuntos
Lesões Encefálicas Traumáticas , Disfunção Cognitiva , Traumatismos Cranianos Fechados , Terapia com Luz de Baixa Intensidade , Animais , Lesões Encefálicas Traumáticas/terapia , Neurônios , RatosRESUMO
Recently, several studies have demonstrated that reactive oxygen species are responsible for inducing multiple organ failure and septic shock. Particularly, mitochondrial dysfunction has been demonstrated in the pathogenesis of multiple organ dysfunction syndrome (MODS). In cytopathic hypoxia, impairment of mitochondrial oxidative phosphorylation decreases aerobic adenosine triphosphate (ATP) production and potentially induces MODS. Shen-Fu (SF) injections are widely used in the treatment of various diseases. SF exhibits cardiovascular protective effects. For example, it can stretch the coronary artery, stabilize blood pressure, regulate IRI, and improve the overall heart function. Clinical studies have demonstrated that SF injections have notable therapeutic effects on septic and hemorrhagic shocks. In the present study, the effects of SF injection on mitochondrial function in the intestinal epithelial cells of rats with endotoxemia were analyzed.
Assuntos
Medicamentos de Ervas Chinesas/farmacologia , Endotoxemia/tratamento farmacológico , Intestino Delgado/efeitos dos fármacos , Mitocôndrias/efeitos dos fármacos , Animais , Citocromos c/metabolismo , Citocinas/sangue , Medicamentos de Ervas Chinesas/administração & dosagem , Endotoxemia/metabolismo , Endotoxemia/patologia , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Injeções Intravenosas , Intestino Delgado/patologia , Masculino , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Mitocôndrias/patologia , Ratos Sprague-DawleyRESUMO
We have found that Fas/FasL-mediated "extrinsic" pathway promoted cell apoptosis induced by renal ischemic injury. This study is to elucidate the upstream mechanism regulating FasL-induced extrinsic pathway during renal ischemia/reperfusion. Results demonstrated that when SIRT2 was activated by renal ischemia/reperfusion, activated SIRT2 could bind to and deacetylate FOXO3a, promoting FOXO3a nuclear translocation which resulted in an increase of nuclear FOXO3a along with FasL expression and activation of caspase8 and caspase3, triggering cell apoptosis during renal ischemia/reperfusion. The administration of SIRT2 inhibitor AGK2 prior to renal ischemia decreased significantly the number of apoptotic renal tubular cells and alleviated ultrastructure injury. These results indicate that inhibition of FOXO3a deacetylation might be a promising therapeutic approach for renal ischemia /reperfusion injury.