Neuroprotective Effects Of Coenzyme Q 10 And Ozone Therapy On Experimental Traumatic Spinal Cord Injuries In Rats.

OBJECTIVE: This study investigates the neuroprotective effects and functional recovery potential of Coenzyme Q10 (CoQ10) and ozone therapy in spinal cord injury (SCI). MATERIAL AND METHODS: In this study, 40 female Sprague-Dawley rats were divided into five groups of eight. Surgical procedures induced spinal cord trauma in all groups, except the control group. The ozone group received 0.7 mg/kg rectal ozone daily for seven days, starting one hour post-spinal cord trauma. The CoQ10 group was administered 120 mg/kg CoQ10 orally once daily for seven days, beginning 24 hours prior to trauma. The CoQ10 + ozone group received both treatments. Examinations included a modified Tarlov scale and inclined plane test on days 1, 3, 5, and 7. Malondialdehyde (MDA) analysis was conducted on serum samples, and assessments of caspase-3, Bcl-2, and Bax levels were performed on tissue samples. Additionally, a comprehensive examination analyzed histopathological and ultrastructural changes. RESULT: After SCI, there was a statistically significant increase in serum MDA, tissue caspase-3, and Bax levels (MDA p<0.001, caspase-3 p<0.001, Bax p=0.003). In the CoQ10 + ozone group, serum MDA (p=0.002), tissue caspase-3 (p=0.001), and Bax (p=0.030) levels were significantly lower compared to the trauma group. Tissue Bcl-2 levels were also significantly higher (p=0.019). The combined treatment group demonstrated improved histopathological, ultrastructural, and neurological outcomes. CONCLUSION: This study shows that CoQ10 + ozone therapy in traumatic SCI demonstrates neuroprotective effects via antioxidant and antiapoptotic mechanisms. The positive effects on functional recovery are supported by data from biochemical, histopathological, ultrastructural, and neurological examinations.

Prospective Randomized Study on the Effects of Improved Sleep Quality After Craniotomy on Melatonin Concentrations and Inflammatory Response in Neurosurgical Intensive Care Patients.

OBJECTIVE: Sleep disorders in intensive care units after a craniotomy can decrease melatonin secretion and increase the inflammatory stress response. The aim of this study was to investigate the influence of improving sleep quality via eye patches and earplugs on melatonin secretion and inflammatory mediator release. METHODS: The study enrolled 41 patients who underwent craniotomy. Patients were randomized into 2 groups. "Group Intervention" received a sleep-promoting intervention with eye patches and earplugs to provide light and noise isolation, while "Group Control" received standard care. Blood levels of C-reactive protein and interleukin 1 and interleukin 6 along with urine levels of 6-sulphatoxymelatonin (aMT6) were measured preoperatively (baseline) and on postoperative days 1 and 3. Sleep quality was assessed with the Richards-Campbell Sleep Questionnaire. RESULTS: Sleep quality was higher in the intervention group (Richards-Campbell score:80.61 ± 11.96 vs. 33.50 ± 16.32; P < 0.001). Urine aMT6 levels increased significantly in the intervention group in spot urine samples from 10.15 (5.38-14.40) ng/mL at baseline to 14.52 (6.24-29.11) and 11.51 (7.88-29.05) ng/mL on postoperative days 1 and 3. They also increased in 24-hour urine samples from 25.73 (8.24-52.73) ng/mL at baseline to 35.38 (11.48-95.65) and 39.18 (2.36-125.23) ng/mL on postoperative days 1 and 3 (P = 0.001 and P = 0.005, respectively). The aMT6 concentration did not change significantly in the control group. The C-reactive protein concentrations increased postoperatively compared with baseline concentrations in both groups (P = 0.001 and P < 0.001). CONCLUSIONS: Melatonin secretion significantly increased as a result of improving postoperative sleep quality by noise and light isolation in neurosurgical intensive care unit patients after craniotomy.

Therapeutic Evaluation of Tumor Necrosis Factor-alpha Antagonist Etanercept against Traumatic Brain Injury in Rats: Ultrastructural, Pathological, and Biochemical Analyses.

PURPOSE: The aim of the present study was to investigate the effect of etanercept (ETA) on histopathological and biochemical changes after traumatic brain injury (TBI) in rats. MATERIALS AND METHODS: Thirty-six male Wistar albino rats were distributed into three groups (n = 12 each). Control group rats were not subjected to trauma. Trauma group rats were subjected to TBI only. ETA group rats were subjected to TBI plus ETA (5 mg/kg intraperitoneal [i.p.]). The groups were further subdivided into those sacrificed in the hyperacute stage (1 h after TBI) (control-1, trauma-1, and ETA-1 groups) and the acute stage (6 h after TBI) (control-6, trauma-6, and ETA-6 groups). Tissue levels of tumour necrosis factor-alpha, interleukin-1 beta, malondialdehyde, catalase, glutathione peroxidase, and superoxide dismutase were analyzed. Histopathological and ultrastructural evaluations were also performed. RESULTS: i.p. administration of ETA at 1 and 6 h significantly reduced inflammatory cytokine expression, attenuated oxidative stress and lipid peroxidation, prevented apoptosis, and increased antioxidant defense mechanism activity in comparison to trauma group. Histopathological and ultrastructural abnormalities were significantly reduced in ETA-treated rats compared to closed head injury trauma groups. CONCLUSIONS: ETA significantly improves neural function and prevents post-TBI histopathological damage in rats.

Stereologic and ultrastructural comparison of human and rat amniotic membrane wrapping for rat sciatic nerve repair.

In this study we aimed to examine the effects on wound healing and nerve regeneration of human and rat amniotic membrane wraps around primary epineural anastomosis areas after a peripheral nerve transection injury in rats. We randomized 25 male adult rats with induced peripheral transection injuries into 5 groups (control, transection injury, primary epineural anastomosis [PEA] after injury, PEA with a human amniotic membrane [hAM] wrap, and PEA with a rat amniotic membrane [rAM] wrap groups and treated their injuries accordingly. We took tissue samples from the anastomosis regions, 12 weeks after the experiment, and analyzed them stereologically and ultrastructurally. We performed a statistical analysis with the recovered stereological counts and the measurement data. Our results showed that the use of amniotic membranes for allografts (between same species) instead of xenografts (between different species), along with microsurgery, provides a suitable microenvironment during the healing process with less immunological reaction on the injured site and supports axonal regeneration.

Etanercept Prevents Histopathological Damage after Spinal Cord Injury in Rats.

BACKGROUND: The aim of our study is to assess the neuroprotective effects of the tumor necrosis factor alpha (TNF-α) inhibitor etanercept (ETA) on histopathological and biochemical changes following spinal cord injury (SCI). PATIENTS AND METHODS: Fifty-four male Wistar albino rats were randomly assigned into three main groups: The sham, trauma, and ETA group (n = 18 per group). Each of these groups was further divided into three subgroups (n = 6 per subgroup) based on the different tissue sampling times postinjury: 1 h, 6 h, and 24 h. Clip compression model was used for SCI. Rats in the ETA group were treated with 5 mg/kg of ETA immediately after the clip was removed. After 1, 6, and 24 h, the spinal cord was totally removed between the levels T8-T10. Sample tissue was immediately harvested and fixed for histopathological and electron microscopic examination and were analyzed for TNF-α, interleukin-1ß (IL-1ß), superoxide dismutase (SOD), adenosine deaminase, catalase (CAT), and malondialdehyde levels in both the tissue and serum. RESULTS: The serum and tissue levels of cytokines and enzymes were seen to change after SCI between hyperacute, acute, and subacute stages. Treatment with ETA selectively inhibited TNF-α, and IL-1ß expression together with increased levels of antioxidative enzymes (SOD, CAT). CONCLUSION: Early administration of ETA after SCI may remarkably attenuate neuronal injury by decreasing tissue and serum TNF-α and IL-1ß levels, while increasing antioxidative enzymes such as SOD and CAT in subacute and acute stages, respectively.

Does Decorin Protect Neuronal Tissue via Its Antioxidant and Antiinflammatory Activity from Traumatic Brain Injury? An Experimental Study.

BACKGROUND: The development of secondary brain injury via oxidative stress after traumatic brain injury (TBI) is well known. Decorin (DC) inactivates transforming growth factor ß1, complement system, and tumor necrosis factor α, which are related to oxidative stress and apoptosis. Consequently, the aim of the present study was to evaluate the role of DC on TBI. METHODS: A total of 24 male rats were used and divided into 4 groups as follows; control, trauma, DC, and methylprednisolone (MP). The trauma, DC, and MP groups were subjected to closed-head contusive weight-drop injuries. Rats received treatment with intraperitoneal saline, DC, or MP, respectively. All the animals were killed at the 24th hour after trauma and brain tissues were extracted. The oxidant/antioxidant parameters (malondialdehyde, glutathione peroxidase, superoxide dismutase, and NO) and caspase 3 in the cerebral tissue were analyzed, and histomorphologic evaluation of the cerebral tissue was performed. RESULTS: Levels of malondialdehyde, NO, and activity of caspase 3 were significantly reduced, and in addition glutathione peroxidase and superoxide dismutase levels were increased in the DC and MP groups compared with the trauma group. The pathology scores and the percentage of degenerated neurons were statistically lower in the DC and MP groups than in the trauma group. CONCLUSIONS: The results of the present study showed that DC inactivates transforming growth factor ß1 and protects the brain tissue and neuronal cells after TBI.

The Surgical Outcome of Traumatic Extraaxial Hematomas Causing Brain Herniation.

AIM: The aim of this study was to assess the surgical outcome and the prognostic importance of clinical and radiological data of patients operated emergently for an extraaxial hematoma causing brain herniation. MATERIAL AND METHODS: This retrospective study comprised 108 adult patients who were operated due to herniated traumatic extraaxial hematomas from January 2000 to January 2013. RESULTS: Of 108 patients, 63 patients (58.3%) were diagnosed as subdural hematoma (SDH), and 45 patients (41.7%) as epidural hematoma (EDH). An unfavorable outcome was significantly increased for patients who were diagnosed as SDH (90.4%) compared with EDH patients (33.3%). Mortality rate for herniated SDH patients was 65.1%, and 26.6% for herniated EDH patients. High mortality and unfavorable outcome ratios were associated with Glasgow Coma Scale scores at admission, mean postoperative intracranial pressure (ICP) values, type of the brain herniation, interval from the time of trauma to the time of hematoma decompression, the duration of the brain herniation, intraoperative acute brain swelling, hematoma volume and thickness, degree of the midline shift and the obliteration of the basal cisterns. CONCLUSION: Our data showed that, postoperative ICP values were one most important predictor of the mortality. We recommended postoperative ICP monitoring for all patients presenting with the brain herniation due to traumatic extraaxial hematoma.

Postoperative seizure following transforaminal percutaneous endoscopic lumbar discectomy.

Endoscopic surgery for lumbar disc herniation has been available for more than 30 years. Transforaminal percutaneous endoscopic lumbar discectomy is a well-known, safe, and effective method used for the treatment of the lumbar disc herniation. The published complications of the transforaminal percutaneous endoscopic lumbar discectomy consist of infections, thrombophlebitis, dysesthesia, dural tear, vascular injury, and death. Seizure after transforaminal percutaneous endoscopic lumbar discectomy is an extremely rare complication. A 20-year-old patient applied at our department who had undergone transforaminal percutaneous endoscopic lumbar. During the procedure, while performing the discography, non-ionic contrast media was administered into the thecal sac inadvertently. Two hours after surgery, the patient developed generalized tonic-clonic seizure of 5-min duration. Diagnosis of iohexol-induced seizure was made and the patient was treated supportively without anti-epileptics. Here we present the first case of seizure after transforaminal percutaneous endoscopic lumbar discectomy, which was caused by inadvertent administration of the contrast media into the thecal sac.

Antioxidant and antiapoptotic effects of darbepoetin-α against traumatic brain injury in rats.

INTRODUCTION: In this study, we tried to determine whether darbepoetin-α would protect the brain from oxidative stress and apoptosis in a rat traumatic brain injury model. MATERIAL AND METHODS: The animals were randomized into four groups; group 1 (sham), group 2 (trauma), group 3 (darbepoetin α), group 4 (methylprednisolone). In the sham group only the skin incision was performed. In all the other groups, a moderate traumatic brain injury modelwas applied. RESULTS: Following trauma both glutathione peroxidase, superoxide dismutase levels decreased (p < 0.001 for both); darbepoetin-α increased the activity of both antioxidant enzymes (p = 0.001 and p < 0.001 respectively). Trauma caused significant elevation in the nitric oxide synthetase and xanthine oxidase levels (p < 0.001 for both). Administration of darbepoetin-α significantly decreased the levels of nitric oxide synthetase and xanthine oxidase (p < 0.001 for both). Also, trauma caused significant elevation in the nitric oxide levels (p < 0.001); darbepoetin-α administration caused statistically significant reduction in the nitric oxide levels (p < 0.001). On the other hand, malondialdehyde levels were increased following trauma (p < 0.001), and darbepoetin α significantly reduced the malondialdehyde levels (p < 0.001). Due to the elevated apoptotic activity following the injury, caspase-3 activity increased significantly. Darbepoetin-α treatment significantly inhibited apoptosis by lowering the caspase-3 activity (p < 0.001). In the darbepoetin group, histopathological score was lower than the trauma group (p = 0.016). CONCLUSIONS: In this study, darbepoetin-α was shown to be at least as effective as methylprednisolone in protecting brain from oxidative stress, lipid peroxidation and apoptosis.

Vasoconstrictive effects of levobupivacaine on the basilar artery in the rabbit.

INTRODUCTION: Spinal anesthesia is a widely used technique of the modern practice of anesthesia. Spinal cord ischemia is a rare but catastrophic complication of spinal anesthesia which may be caused by a direct vasoconstrictive effect of the local anesthetic. Although the vasoconstrictive effects of levobupivacaine have been widely studied, the vasoconstrictive effects of this drug on the intradural arteries have never been studied. The aim of this study is to evaluate whether levobupivacaine has vasoconstrictive effects on the basilar artery in rabbits. MATERIAL AND METHODS: Thirty male New Zealand white rabbits were divided randomly into three groups of ten rabbits each: group 1 (control); group 2 (0.125% levobupivacaine); group 3 (0.25% levobupivacaine). The cisterna magna was punctured as described below, then 1 ml of saline or 0.125% or 0.25% levobupivacaine was injected into the cisterna magna in 10 min by an infusion pump in groups 1, 2 and 3 respectively. All animals were euthanized by perfusion-fixation 30 min after the procedure. The luminal area and the size of the cross-sectional area for each basilar artery were measured. RESULTS: Both 0.125% and 0.25% levobupivacaine infusion caused significant vasoconstriction. Vasoconstriction was more significant for the 0.125% concentration. CONCLUSIONS: The results of this study indicated that both 0.125% and 0.25% concentrations of levobupivacaine caused significant vasoconstriction of the basilar artery when administered into the subarachnoid space. This may constitute proof that subarachnoid administration of levobupivacaine may diminish the spinal cord blood flow, causing ischemia.

Therapeutic evaluation of interleukin 1-beta antagonist Anakinra against traumatic brain injury in rats.

BACKGROUND: The aim of this study was to evaluate the therapeutic efficiency of Anakinra, an IL-1ß antagonist with anti-inflammatory effects, in an experimental model of traumatic brain injury (TBI). METHODS: Fifty-four rats underwent TBI after a weighted object was dropped onto a metal disc secured to their skulls. Animals were randomized into 3 main groups: control (n=18), TBI + saline (n=18; six animals per time-point) with samples obtained at the first, sixth and twenty-fourth h postoperatively, and TBI + Anakinra (n=18; six animals per time-point) with brain samples obtained at the first, sixth and twenty-fourth h postoperatively. Brain tissue and blood serum were extracted for the analysis of IL-1ß, malondialdehyde, glutathione peroxidase, superoxide dismutase, and catalase levels. Tissue sections were evaluated histopathologically under a light microscope. RESULTS: After trauma, tissue and serum IL-1ß levels were significantly elevated and after Anakinra administration, these levels substantially decreased. Glutathione peroxidase, superoxide dismutase, and catalase activity decreased following TBI and Anakinra administration proved effective in increasing the activity of these antioxidant enzymes. Histopathological analysis confirmed that Anakinra might protect the brain tissue and nerve cells from injury. CONCLUSION: Results demonstrate that Anakinra reduces the development of inflammation and tissue injury events associated with TBI.

The histopathological and ultrastructural effects of the topical application of bacitracin on the cerebral cortex in rats.

AIM: Bacitracin is one of the most frequently used agents for the topical irrigation of the cerebral cortex. The aim of this study is to investigate whether bacitracin has histopathological and ultrastructural effects when applied topically to the cerebral cortex. MATERIAL AND METHODS: Twenty-eight rats were randomly assigned to four groups. Except the control group, each rat underwent left frontoparietal craniectomy with dural removal. Then, in the sham group a piece of dry absorbable gelatin sponge was placed over the left hemisphere; in the saline group a gelatin sponge soaked in normal saline; and in the bacitracin group a gelatin sponge soaked in 500 units bacitracin was used. After 48 hours, brain tissues were extracted for histopathological and electron microscopic analyses. RESULTS: Among the four groups dark stained neurons were found to be statistically higher in number in the bacitracin group compared with the control, sham and saline groups. Electron microscopic evaluation revealed that, in the bacitracin group, almost all cytoplasmic organelles were poorly preserved. CONCLUSION: Topical application of the bacitracin on to the cerebral cortex caused histopathological and ultrastructural changes in the neural tissue. These changes may be an evidence for the neurotoxic effects of bacitracin.

Neuroprotective effects of testosterone on ischemia/reperfusion injury of the rabbit spinal cord.

AIM: Previous studies demonstrated the neuroprotective effects of testosterone, but no previous study has examined the neuroprotective effects of testosterone on spinal cord ischemia/reperfusion injury. The purpose of this study was to evaluate whether testosterone could protect the spinal cord from ischemia/reperfusion injury. METHODS: Rabbits were randomised into four groups of eight animals as follows: group 1 (control), group 2 (ischemia), group 3 (methylprednisolone) and group 4 (testosterone). In the control group only a laparotomy was performed. In all other groups, the spinal cord ischemia model was created by the occlusion of the aorta just caudal to the renal artery. Levels of malondialdehyde and catalase were analysed, as were the activities of caspase-3, myeloperoxidase, and xanthine oxidase. Histopathological and ultrastructural evaluations were performed. Neurological evaluation was performed with the Tarlov scoring system. RESULTS: After ischemia-reperfusion injury, increases were found in caspase-3 activity, myeloperoxidase activity, malondialdehyde levels, and xanthine oxidase activity. In contrast, decreases in catalase levels were observed. After the administration of testosterone, decreases were observed in caspase-3 activity, myeloperoxidase activity, malondialdehyde levels, and xanthine oxidase activity, whereas catalase levels increased. Furthermore, testosterone treatment showed improved results concerning histopathological scores, ultrastructural score and Tarlov scores. CONCLUSIONS: Our results revealed for the first time that testosterone exhibits meaningful neuroprotective activity following ischemia-reperfusion injury of the spinal cord.

The comparative effects of recombinant human erythropoietin and darbepoetin-alpha on cerebral vasospasm following experimental subarachnoid hemorrhage in the rabbit.

BACKGROUND: Darbepoetin alpha is a hypersialylated analogue of erythropoietin effective for activating erythropoietin-receptors. This study investigated the vasodilator and neuroprotective effects of darbepoetin alpha on an experimental subarachnoid hemorrhage model and compared it with erythropoietin. METHODS: Forty adult male New Zealand white rabbits were randomly divided into four groups of ten rabbits each: group 1 (control), group 2 (subarachnoid hemorrhage), group 3 (erythropoietin), and group 4 (darbepoetin alpha). Recombinant human erythropoietin was administered at a dose of 1,000 U/kg intraperitoneally after the induction of subarachnoid hemorrhage and continued every 8 h up to 72 h. Darbepoetin alpha was administered at a single intraperitoneal dose of 30 µg/kg. Animals were killed 72 h after subarachnoid hemorrhage. Basilar artery cross-sectional areas, arterial wall thicknesses, hippocampal degeneration scores and biochemical analyses were measured in all groups. RESULTS: Both erythropoietin and darbepoetin alpha treatments were found to attenuate cerebral vasospasm and provide neuroprotection after subarachnoid hemorrhage in rabbits. Darbepoetin alpha revealed better morphometric and histopathological results than erythropoietin among experimental subarachnoid hemorrhage-induced vasospasm. CONCLUSIONS: Our findings, for the first time, showed that darbepoetin alpha can prevent vasospasm and provides neuroprotection following experimental subarachnoid hemorrhage. Moreover, darbepoetin alpha showed better results when compared with erythropoietin.

Giant intradiploic epidermoid cyst presenting as solitary skull mass with intracranial extension.

Epidermoid cysts are rare benign tumors that constitute 0.3% to 1.8% of all intracranial tumors. They are inclusion tumors that include epidermoid elements and are most commonly located in the cerebellopontine angle cistern and the parasellar region, and their location in the diploic space is very rare. These lesions slowly grow and usually do not involve the intracranial compartment. In this article, a case of giant epidermoid cyst located in the left frontal intradiploic space is presented with clinical, radiologic features and surgical treatment.

The protective effect of low-dose methotrexate on ischemia-reperfusion injury of the rabbit spinal cord.

Methotrexate was developed as a cytostatic agent, but at low doses, it has shown potent anti-inflammatory activity. Previous studies have demonstrated that the anti-inflammatory effects of methotrexate are primarily mediated by the release of adenosine. In this study, we hypothesized that low-dose methotrexate has protective effects in spinal cord ischemia-reperfusion injury. Rabbits were randomized into the following four groups of eight animals each: group 1 (control), group 2 (ischemia), group 3 (methylprednisolone) and group 4 (methotrexate). In the control group only a laparotomy was performed. In all the other groups, the spinal cord ischemia model was created by the occlusion of the aorta just caudal to the renal artery. Neurological evaluation was performed with the Tarlov scoring system. Levels of myeloperoxidase, malondialdehyde and catalase were analyzed, as were the activities of xanthine oxidase and caspase-3. Histopathological and ultrastructural evaluations were also performed. After ischemia-reperfusion injury, increases were found in the serum and tissue myeloperoxidase levels, tissue malondialdehyde levels, xanthine oxidase activity and caspase-3 activity. In contrast, both serum and tissue catalase levels were decreased. After the administration of a low-dose of methotrexate, decreases were observed in the serum and tissue myeloperoxidase levels, tissue malondialdehyde levels, xanthine oxidase activity and caspase-3 activity. In contrast, both the serum and tissue catalase levels were increased. Furthermore, low-dose methotrexate treatment showed improved results concerning the histopathological scores, the ultrastructural score and the Tarlov scores. Our results revealed that low-dose methotrexate exhibits meaningful neuroprotective activity following ischemia-reperfusion injury of the spinal cord.

Solitary dural plasmacytoma mimicking meningioma and invading calvarium.

Solitary plasmacytoma comprises 2%-10% of all plasma cell diseases. Cranial localization of plasmacytoma is quite rare. They may emerge after years without systemic involvement and symptoms. They may be confused with other tumors as they are not remembered primarily in radiological diagnosis. The definite diagnosis is made upon histopathological examination. Surgical resection followed by radiotherapy is the first choice of therapy. Chemotherapy may be administered for secretory tumors. In this paper, we discussed a patient who underwent surgery with the prediagnosis of meningioma and histopathologically diagnosed with plasmacytoma.

An unusual sacral osteomyelitis due to an occult anterior sacral meningocele.

OBJECTIVE: We present the extremely rare case of sacral osteomyelitis due to an anterior sacral meningocele (ASM) with fistula to the skin. We also discuss the case's clinical significance and the importance of imaging in diagnosis. METHODS: A 28-year-old female patient was referred to our clinic due to back and hip pain, erythema, and purulent discharge from the right gluteal region. Neurological examination was normal except for pain in the gluteal region. Physical examination revealed a porus lateral to the right gluteal region. Lumbar magnetic resonance imaging (MRI)showed osteomyelitis and a minimal occult sacral meningocele in the anterior sacral region. Contrast-enhanced radiographic imaging clearly showed the fistula tract. The patient underwent surgery via the posterior approach; debridement of the sacral osteomyelitis was performed and the fistula tract toward the skin was closed. RESULTS: She was pain free after surgery. There were no postoperative complications. CONCLUSION: Although vertebral osteomyelitis due to ASMs is extremely rare, the risk of infection increases in cases of a fistula to the skin. When investigating the etiology of treatment-resistant infections, especially of the skin, sacral osteomyelitis and an underlying anomaly must be kept in mind.

The protective effect of 2-mercaptoethane sulfonate (MESNA) against traumatic brain injury in rats.

BACKGROUND: The agent, 2-mercaptoethane sulfonate (MESNA), is a synthetic small molecule, widely used as a systemic protective agent against chemotherapy toxicity, but is primarily used to reduce hemorrhagic cystitis induced by cyclophosphamide. Because MESNA has potential antioxidant and cytoprotective effects, so we hypothesized that MESNA may protect the brain against traumatic injury. METHOD: Thirty-two rats were randomized into four groups of eight animals each; Group 1 (sham), Group 2 (trauma), Group 3 (150 mg/kg MESNA), Group 4 (30 mg/kg methylprednisolone). Only skin incision was performed in the sham group. In all the other groups, the traumatic brain injury model was created by an object weighing 450 g falling freely from a height of 70 cm through a copper tube on to the metal disc over the skull. The drugs were administered immediately after the injury. The animals were killed 24 h later. Brain tissues were extracted for analysis, where levels of tissue malondialdehyde, caspase-3, glutathione peroxidase, superoxide dismutase, nitric oxide, nitric oxide synthetase and xanthine oxidase were analyzed. Also, histopathological evaluation of the tissues was performed. RESULTS: After head trauma, tissue malondialdehyde levels increased; these levels were significantly decreased by MESNA administration. Caspase-3 levels were increased after trauma, but no effect of MESNA was determined in caspase-3 activity. Following trauma, both glutathione peroxidase and superoxide dismutase levels were decreased; MESNA increased the activity of both these antioxidant enzymes. Also, after trauma, nitric oxide, nitric oxide synthetase and xanthine oxidase levels were increased; administration of MESNA significantly decreased the levels of nitric oxide, nitric oxide synthetase and xanthine oxidase, promising an antioxidant activity. Histopathological analysis showed that MESNA protected the brain tissues well from injury. CONCLUSIONS: Although further studies considering different dose regimens and time intervals are required, MESNA was shown to be at least as effective as methylprednisolone in the traumatic brain injury model.