RESUMO
Neuronal cell apoptosis is associated with various factors that induce neurological damage, including radiation exposure. When administered prior to exposure to radiation, a protective agent may prevent cellular and molecular injury. The present study aimed to investigate whether melatonin exerts a neuroprotective effect by inhibiting the caspase cell death pathway. Male Sprague-Dawley rats were administered melatonin (100 mg/kg body weight) 30 min prior to radiation exposure in red light during the evening. In order to elucidate whether melatonin has a neuroprotective role, immunohistochemistry, terminal deoxynucleotidyl transferase dUTP nick-end labeling, Nissl staining, reverse transcription-quantitative polymerase chain reaction, reactive oxygen species analysis and western blotting were performed. At 24 h post-melatonin treatment, caspase-3 mRNA and protein expression levels were significantly decreased. These results demonstrated that melatonin may protect hippocampal neurons via the inhibition of caspase-3 when exposed to irradiation. Therefore, caspase-3 inhibition serves a neuroprotective and antioxidant role in the interventional treatment of melatonin. The results of the present study suggested that melatonin may have a potential therapeutic effect against irradiation; however, further studies are required in order to elucidate the underlying antioxidant mechanisms.
RESUMO
Resveratrol, a naturally occurring phytoalexin, acts as an activator of sirtuin 1 (SIRT1) and has been shown to have a neuroprotective role in various models. Healthy adult male Sprague-Dawley rats were subjected to cerebral ischemia in order to study the protective effect of resveratrol on the brain following ischemia, and to investigate the effects of SIRT1 activation on the hippocampus. Untreated and resveratrol-treated rats were anesthetized prior to undergoing surgery to induce middle cerebral artery occlusion followed by reperfusion. SIRT1 expression was evaluated by immunohistochemistry, western blotting and reverse transcription-quantitative polymerase chain reaction, and SIRT1 activity was also evaluated. In addition, terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) and Nissl staining assays were conducted and the levels of reactive oxygen species were determined. It was observed that resveratrol significantly decreased the number of TUNEL-positive cells and increased the expression of SIRT1 mRNA in a dose-dependent manner. This was accompanied by increases in SIRT1 protein expression levels and SIRT1 activity. The results demonstrate the neuroprotective and antioxidant effects of resveratrol against ischemia-induced apoptosis in the rat hippocampus.
RESUMO
It has been recognized that radiation-induced effects remain a significant risk. An accumulation of reactive oxygen species (ROS) is considered to be one factor that contributes to neurodegenerative changes. The aim of our study was to investigate the potential radioprotective effects of NAC. Male Sprague-Dawley rats underwent radiation. Irradiation was performed at room temperature with a 4-Gy dose of radiation. A dose of N-acetylcysteine (NAC) was performed 15 min prior to irradiation intraperitoneally. The methods of immunohistochemistry, TUNEL staining, Nissl staining, qRT-PCR, analysis of reactive oxygen species and Western blot were performed. In conclusion, our results demonstrate that NAC inhibits apoptosis induced by irradiation via the inhibition of caspase-3. We demonstrated a decrease in caspase-3 mRNA that was present at 24h of NAC treatment. Such mRNA decrease was accompanied by a decrease of protein. In the present study, NAC effectively antagonized oxidation induced by irradiation. These results provide evidence that the neural protective effect and the antioxidant effect of NAC contribute to metabolic activity.