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Background and purpose: Vitamin C and CoQ10 are known as two potentantioxidants. We studied the protective Role of CoQ10 and ascorbic acid against Ischemia-Reperfusion. Finally, we have compared the therapeutic effect of these two together. Materials and methods: 35 male balb-Cwere divided into seven subgroups. Includes five groups: intact, ischemicControl, sham Control and treatment groups with CoQ10 and treatment groups with ascorbic acid. In treatment groups, the mice treated with CoQ10 and vitC as Pre-Treatment for a week. Then, ischemia induced by Common Carotid artery ligation. The mice post-treated with CoQ10and ascorbic acidfor a week. Nissl staining applied to counting necroticCells of hippocampus. TUNNEL kit was used to quantify apoptoticCell death while to short term memory scale, we apply y-maze and shuttle box tests. Results: High rate of apoptosis was seen in ischemic group associated with significantly short-term memory loss. In the treatment groups withthese antioxidants, Cell death was significantly lower than the ischemic Control group. Between treatment groups, group treated with CoQ10 was less neuronal death than the group treated with ascorbic acid. Conclusion: According to the results of this study, ascorbic acid and CoQ10 intake significantly reduced Cell death and decreased memory loss. Butthe antioxidant effect of CoQ10 is stronger than vitamin C in this zone of brain.

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Background and purpose: Recent studies have demonstrated the promising effects of mesenchymal stem cells (MSCs) in some neurodegenerative diseases and proved their neuroprotective effects. But, the detailed pathways and the ability of MSCs from various sources has not been fully investigated.
Materials and methods: Here, we isolated MSCs from two sources; adipose tissue and dental pulp, and compared the neuroprotective effects of adipose derived stem cells-conditioned media (ADSCs-CM) and dental pulp derived stem cells-conditioned media (DPSCs-CM) on SH-SY5Y cells exposed to Cobaltous chloride(CoCl2) as a model of hypoxia-induced neural damage. SH-SY5Y cells exposed to CoCl2 were treated with ADSCs-CM and DPSCs-CM and the cell viability, apoptosis, and cellular damage were determined by AlamarBlue ^®assay, propidium iodide (PI) test, and lactate dehydrogenase (LDH) assay, respectively.
Results: According to AlamarBlue® results, both ADSCs-CM and DPSCs-CM showed protective effects on SH-SY5Y cells exposed to CoCl₂ at 0.6 mM for 12 and 24 h. Furthermore, ADSCs-CM could protect SH-SY5Y cells against hypoxic condition more intensively at all CoCl₂ concentrations and various incubation incubation periods (P<0.01 and P<0.001, respectively). However, there were no significant differences between ADSCs-CM and DPSCs-CM. Also, ADSCs-CM and DPSCs-CM could considerably reduce the LDH release and apoptotic cells when SH-SY5Y cells were exposed to 0.6 mM CoCl₂ for 24 h.
Conclusion: The study indicated that both ADSCs-CM and DPSCs-CM have neuroprotective effects on hypoxic SH-SY5Y cells through reduction of apoptotic cells and release of LDH.

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 Background and purpose: Allicin has a wide range of pharmacological functions, all of which can be demonstrated in anti-inflammatory, antioxidant, antifungal and anti-tumor activities. In this research, we investigated the neuroprotective role of allicin in the process of diffuse traumatic brain injury and its effect on interleukin levels and histological changes in rats.
Materials and methods: In this experimental study, Wistar rats (n=56) underwent diffuse controlled brain injury by Marmarou method, and 30 minutes later, the drug was injected intraperitoneally at different doses. Veterinary Coma Scale was used and Beam Walk and Beam Balance movement and balance tests were taken at pre-traumatic times, immediately after recovery from the trauma, and 24, 48, and 72 hours after the trauma.
Results: Findings showed that allicin at 25 mg/kg and 50 mg/kg can reduce these differences compared to the control group (Sham and Intact) (P<0.001). Allicin was found to be more effective at 25 mg/kg (P<0.0001).
Conclusion: Allicin showed neuroprotective effects in the brain and can affect the consequences of trauma, reduce cerebral edema, accelerate improvement of blood-brain barrier, and improve neurological scores and the function of vestibular system.
 

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Background and purpose: Traumatic brain injury (TBI) is one of the most complex diseases of the central nervous system (CNS). Nesfatin is an 82-amino acid effective polypeptide in CNS. In this study, we investigated the role of nesfatin in neuron protection in the process of diffuse concussion in rats and also its effect on the level of matrix metalloproteinase-9.
Materials and methods: In this experimental study, 56 Wistar rats were subjected to TBI by the Marmaru method. After 30 minutes, nesfatin was injected intraperitoneally at different doses, and repeated on second and third days. The results of Veterinary Coma Scale, beam walk and beam balance tests were recorded at Pre-TBI, immediately after TBI, 24, 48, and 72 hours after TBI. After 72 hours, CSF was collected from the cisterna magna and used for ELISA test to measure the matrix metalloproteinase-9.
Results: Intraperitoneal administration of nesfatin at 50 µg/kg and 10 µg/kg can reduce cerebral edema, destruction of the blood-brain barrier, and neurological and balance-motor scores (P<0.0001) compared with the control group (Sham and Intact) (P<0.0001). Nesfatin was not found effective at 20µg/kg (P>0.05).
Conclusion: Nesfatin has been able to affect the consequences of trauma and reduce brain edema, accelerate the improvement of blood-brain barrier and neurological and balance scores. Probably part of these neuroprotective effects is through reduction of MMP-9.