ABSTRACT
MDMA (3,4-Methylenedioxymethamphetamine) is a common recreational drug of abuse which causes neurodegeneration. Nicotine and modafinil provide antioxidant and neuroprotective properties and may be beneficial in the management of MDMA-induced neurotoxicity. The purpose of this study was to characterize how acute and chronic administration of nicotine and/or modafinil exert protective effects against the MDMA-induced impaired cognitive performance, oxidative stress, and neuronal loss. Adult male rats were divided into three groups, namely control, MDMA and treatment (modafinil and/or nicotine). MDMA (10 mg/kg) was administered intraperitoneally during a three-week schedule (two times/day for two consecutive days/week). The treated-groups were classified based on the acute or chronic status of treatment. In the groups which underwent acute treatments, nicotine (0.5 mg/kg) and/or modafinil (100 mg/kg) were injected just prior to the MDMA administration (acute nicotine (NA), acute modafinil (MA), and acute nicotine and modafinil (NMA)). In the rats which received chronic treatments, nicotine (0.5 mg/kg) and/or modafinil (100 mg/kg) were injected every day during the three week-schedule administration of MDMA (chronic nicotine (NC), chronic modafinil (MC), and chronic nicotine and modafinil (NMC)). Learning and memory performance, as well as avoidance response, were assessed by Morris water maze and Shuttle box, respectively. Our findings indicate enhanced learning and memory and avoidance response in the NMC group. By TUNEL test and Cresyl Violet staining we evaluated neuronal loss and apoptosis in the hippocampal CA1 and found increased neuronal viability in the NMC group. On the other hand, chronic administration of modafinil and nicotine significantly down-regulated the caspase 3 and up-regulated both BDNF and TrkB levels in the MDMA-received rats. The serum levels of glutathione peroxidase (GPx) and total antioxidant capacity (TAC) were evaluated and we found that the alterations of serum levels of GPx and TAC were considerably prevented in the NMC group. The overall results indicate that nicotine and modafinil co-administration rescued brain from MDMA-induced neurotoxicity. We suggest that nicotine and modafinil combination therapy could be considered as a possible treatment to reduce the neurological disorders induced by MDMA.
Subject(s)
Hippocampus/drug effects , Modafinil/administration & dosage , N-Methyl-3,4-methylenedioxyamphetamine/toxicity , Neurons/drug effects , Neuroprotection/drug effects , Nicotine/administration & dosage , Animals , Antioxidants/administration & dosage , Avoidance Learning/drug effects , Avoidance Learning/physiology , Drug Therapy, Combination , Hallucinogens/toxicity , Hippocampus/pathology , Male , Maze Learning/drug effects , Maze Learning/physiology , Neurons/pathology , Neuroprotection/physiology , RatsABSTRACT
INTRODUCTION: The administration of 3,4-methylenedioxymethamphetamine (MDMA) or ecstasy causes memory impairment, whereas neurogenesis improves memory and learning. Hence, this study evaluated the effects of MDMA on neurogenesis in the hippocampus of male rats. METHODS: Adult male Wistar rats received Intraperitoneal (IP) injections of MDMA (10 mg/ kg). We assessed nestin, sex-determining region Y-box 2 (Sox2), and NeuroD expressions according to the immunohistochemistry analyses. RESULTS: MDMA reduced the expressions of nestin, Sox2, and NeuroD compared with the control groups. The reduction in NeuroD expression was age-related. CONCLUSION: MDMA possibly has negative effects on neurogenesis, which specifically results from impaired survival of newborn cells.
ABSTRACT
Introduction: Wound healing is a dynamic, interactive process to achieve the restoration of skin integrity and proper function after damage. Applying a low-level laser (LLL) and light emitting diodes (henceforth LEDs) is introduced in previous studies to accelerate the process of wound healing. The aim of this study is to compare the effect of the LLL and LEDs on wound healing in rabbits. Methods: Full thickness same size square excision wounds were created on the dorsum of the rabbits. Twenty rabbits were randomly divided into four groups, according to the treatment received. Group 1: the AlGalInP (aluminium gallium indium phosphide) laser (4 J/cm²); group 2: the red LED (30 J/cm²); group 3: the blue LED (60 J/cm²) and group 4, as the control group, was not irradiated. After 30 days, the wounds were evaluated both morphologically and histopathologically. Statistical significance was defined as a P value of less than 0.05. Results: All interfering methods including the LLL and LEDs had better outcome compared with the control group of both sizes and histopathologic features. The red laser group showed better results compared to the control group and either the LED groups. Comparing LEDs, the red LED performed better than the blue LED. Conclusion: This study confirmed the significant effects of the LLL and LEDs on wound healing. Comparing the LLL and LED, the LED may be a better choice, especially for bedridden or debilitated patients. The LED may also more cost effective in wound healing in comparison with the LLL.