Atorvastatin efficiency after traumatic brain injury in rats

Türkoğlu, Ömer Faruk; Eroğlu, Hakan; Okutan, Özerk; Gurcan, Oktay; Bodur, Ebru; Sargon, Mustafa F.; Öner, Levent; Beşkonaklı, Etem

doi:10.1016/j.surneu.2008.07.004

Cited by 27 publications

(17 citation statements)

References 35 publications

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“…In trauma, free radicals and iron compounds catalyze not only the generation of hydroxyl radical and cause lipid peroxidation but also increases pro-inflammatory cytokines such as TNF-α, IL-1 β and IL-6 (22). The results in this study clearly confirm that trauma increases the levels of MDA, TNF-α and IL-6 in the spinal cord of rats at 24 hours after injury.…”

Section: █ Discussionsupporting

confidence: 74%

Comparative biochemical and motor function analysis of alpha lipoic acid and n-acetyl cysteine treatment on rats with experimental spinal cord injury

Gürçay

Gurcan²,

Kazanci³

et al. 2015

Turkish Neurosurgery

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SCI develops in two phases: primary and secondary injury. The mechanical impact of the trauma destroys neurons and disrupts the architecture of the tissue, composing the primary phase, but it also induces the overproduction of deleterious substances, which provokes the secondary injury cascade (13).For the secondary injury cascade, numerous distinct mechanisms have been hypothesized and analyzed. The activation of microglia and oxidative stress are the pivotal secondary injury mechanisms after traumatic injury that construct the █ INTRODUCTION Neuro-trauma is one of the most devastating health care and social problems in both developed and underdeveloped countries. Spinal cord injury (SCI) constitutes a major portion of neuro-traumas. Global prevalence of SCI varies from 236 to 1.280 per million inhabitants (6). An enormous amount of resources and manpower has been made available to reverse the effects of SCI. The processes, which have been investigated for ameliorating the results of the injury, have been the target of novel treatments.AIm: Spinal Cord Injury (SCI) is a devastating health problem both for the patient and the clinician. Numerous treatment modalities have been studied to reverse the effects of spinal cord injury. Herein is reported the effects and the comparison of Alpha Lipoic Acid and N-Acetyl Cysteine on rats with SCI. mATERIAl and mEThODS: 38 adult male Sprague-Dawley rats were randomly divided into 5 groups: only laminectomy, laminectomy and trauma, laminectomy trauma and Alpha Lipoic Acid 100 mg/kg IP administration, laminectomy trauma and N-Acetyl Cysteine 300 mg/kg IP administration, and vehicle group (PEG). The trauma model was the Modified Allen Weight drop method. After the procedure, the rats' motor function was evaluated using the modified Tarlov Scale and consequently they were sacrificed and the spinal cord tissue was analyzed biochemically for inflammation markers.RESUlTS: Both Alpha Lipoic Acid and N-Acetyl Cysteine administration after the injury significantly improved the results. There was no statistically significant difference in between the agents. CONClUSION: Although these agents both proven to be effective in ameliorating the effects of SCI, there was not enough evidence in this research to conclude the benefit of one agent over the other.

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Section: █ Discussionsupporting

confidence: 74%

Comparative biochemical and motor function analysis of alpha lipoic acid and n-acetyl cysteine treatment on rats with experimental spinal cord injury

Gürçay

Gurcan²,

Kazanci³

et al. 2015

Turkish Neurosurgery

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“…A modified controlled cortical impact device (VA, USA) was used to administer unilateral brain injury based on the modified Feeney method [20]. Briefly, rats were anesthetized with chloral hydrate (360 mg/ kg, i.p.).…”

Section: Tbi Modelingmentioning

confidence: 99%

Bone Marrow Stromal Cells Promote Neuronal Restoration in Rats with Traumatic Brain Injury: Involvement of GDNF Regulating BAD and BAX Signaling

Shen¹,

Yin²,

Xia³

et al. 2016

Cell Physiol Biochem

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Background/Aims: To investigate the effects of bone marrow stromal cells (BMSCs) and underlying mechanisms in traumatic brain injury (TBI). Methods: Cultured BMSCs from green fluorescent protein-transgenic mice were isolated and confirmed. Cultured BMSCs were immediately transplanted into the regions surrounding the injured-brain site to test their function in rat models of TBI. Neurological function was evaluated by a modified neurological severity score on the day before, and on days 7 and 14 after transplantation. After 2 weeks of BMSC transplantation, the brain tissue was harvested and analyzed by microarray assay. And the coronal brain sections were determined by immunohistochemistry with mouse anti-growth-associated protein-43 kDa (anti-GAP-43) and anti-synaptophysin to test the effects of transplanted cells on the axonal regeneration in the host brain. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and Western blot were used to detect the apoptosis and expression of BAX and BAD. Results: Microarray analysis showed that BMSCs expressed growth factors such as glial cell-line derived neurotrophic factor (GDNF). The cells migrated around the injury sites in rats with TBI. BMSC grafts resulted in an increased number of GAP-43-immunopositive fibers and synaptophysin-positive varicosity, with suppressed apoptosis. Furthermore, BMSC transplantation significantly downregulated the expression of BAX and BAD signaling. Moreover, cultured BMSC transplantation significantly improved rat neurological function and survival. Conclusion: Transplanted BMSCs could survive and improve neuronal behavior in rats with TBI. Mechanisms of neuroprotection and regeneration were involved, which could be associated with the GDNF regulating the apoptosis signals through BAX and BAD.

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“…16,18,19 In cultures of human BBB endothelia, lovastatin and simvastatin were shown to decrease the translocation of both albumin and sucrose, but not normal leukocytes. 20 Microglia (i.e., the resident immune cells of the brain) are implicated in the secretion of glutamate, reactive oxygen species, and other inflammatory mediators, which may exacerbate cerebral edema and secondary neuronal injury.…”

Section: Effects On Inflammation and Excitotoxicitymentioning

confidence: 99%

Statins in Traumatic Brain Injury

Wible

Laskowitz

2010

Neurotherapeutics

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Summary: Traumatic brain injury (TBI) is a common cause of long-term neurological morbidity, with devastating personal and societal consequences. At present, no pharmacological intervention clearly improves outcomes, and therefore a compelling unmet clinical need remains. 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or "statins," offer a potential novel therapeutic strategy for TBI. Statins are well tolerated, easy to administer, and have a long clinical track record in critically ill patients. Their side effects are well defined and easily monitored. Preclinical studies have shown significant benefit of statins in models of TBI and related disease processes, including cerebral ischemia, intracerebral hemorrhage, and subarachnoid hemorrhage. In fact, multiple mechanisms have been defined by which statins may exert benefit after acute brain injury. Statins are currently positioned to be translated into clinical trials in acute brain injury and have the potential to improve outcomes after TBI.

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Atorvastatin efficiency after traumatic brain injury in rats

Cited by 27 publications

References 35 publications

Comparative biochemical and motor function analysis of alpha lipoic acid and n-acetyl cysteine treatment on rats with experimental spinal cord injury

Comparative biochemical and motor function analysis of alpha lipoic acid and n-acetyl cysteine treatment on rats with experimental spinal cord injury

Bone Marrow Stromal Cells Promote Neuronal Restoration in Rats with Traumatic Brain Injury: Involvement of GDNF Regulating BAD and BAX Signaling

Statins in Traumatic Brain Injury

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