Antioxidant-based neuroprotective effect of dimethylsulfoxide against induced traumatic brain injury in a rats model

Abstract

Traumatic brain injury (TBI) has been the result of neurological deficit and oxidative stress. This study evaluated the antioxidative neuroprotective property and learning and memory-enhancing effects of dimethyl sulfoxide (DMSO) in a rat model after the induction of TBI. 21 albino rats with 7 rats per group were used in this study. Group I was induced with TBI and treated with DMSO at 67.5 mg/kg orally once daily which started 30 min after the induction of TBI and lasted 21 days. Group II was induced with TBI but not treated while Group III was neither induced with TBI nor treated. Assessment of behavioral function (Learning and memory, anxiety and motor function), the level of an antioxidant enzymes and their gene expression (superoxide dismutase, catalase, glutathione peroxidase), the biomarkers of oxidative stress (malondialdehyde) and S100B levels as well as brain tissues histological studies were conducted. Administration of DMSO to rats with induced TBI has improved learning and memory, locomotor function and decreased anxiety in Group I compared to Group II. Moreover, the level of S100B was significantly (p < 0.05) lower in Group I compared to Group II. Treatment with DMSO also decreased lipid peroxidation significantly (p < 0.05) compared to Group II. There exists a significant (p < 0.05) increase in CAT, SOD, and GPX activities in Group I compared to Group II. Therefore, DMSO has demonstrated a potential antioxidative neuroprotective effect through its ability to increase the level of antioxidant enzymes which they quench and inhibit the formation of ROS, thereby improving cognitive functions.

Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets

“…Research with animal TBI models indicates that focusing on secondary injury mechanisms could yield treatments that significantly improve cognitive functions [107,108]. These findings provide a fresh perspective on TBI treatment, underscoring the need for a multifaceted approach to tackle different facets of neuronal damage and recovery.…”

Autologous Cord Blood vs Individualized Supplements in Autistic Spectrum Disease – Results of the CORDUS Study

“…Besides being a vital cryoprotectant DMSO also has a multitude of actions at cellular and molecular level: acts as antioxidant (13,14), prevents accumulation of DNA breakage and facilitates DNA damage repair (15)(16)(17), is neuroprotective via decreasing glutamate and NMDA activation (18), has positive actions on neurons (19), modifies the blood-brain barrier permeability, decreases thrombosis with other vascular actions (20)(21)(22)(23)(24), induces stem cell differentiation into neuronal precursors via activation of necessary intracellular pathways (25)(26)(27)(28)(29); inhibits the pro-inflammatory function of leukocytes, including TNF-alpha function (30) and has other immunomodulatory actions (31)(32)(33)(34)(35). Because of its inhibitory action on leukocytes DMSO is "washed" from the cryopreserved grafts used for hematopoietic reconstitution (in hematology-oncology transplants), however intracellular DMSO cannot be removed and its metabolites are still felt after its administration in patients' breath.…”

Effect of Vitamin E on Serum MDA and Antioxidant Enzymes in Traumatic Brain Injury-Induced Rats

“…Secondary injuries aggravate the damage caused by TBI [13], through a cascade of mechanisms that leads to long-term or life-long difficulties [14] and even mortality [15]. Mechanisms such as hypoxia, glutamate excitotoxicity, disruption of the blood-brain barrier (BBB), calcium overload, mitochondrial dysfunction, and neuro-inflammation all contribute to cell death via necrosis or apoptosis [15, 16,].…”