Prevention of reperfusion injury of the spinal cord in aortic surgery: An experimental study

Koçoğulları, Cevdet Uğur; Becit, Necip; Erkut, Bilgehan; Keleş, Mevlüt Sait; Ceviz, Münacettin; Ateş, Azman; Gündoğdu, Cemal; Kayğın, Mehmet Ali; Koçak, Hikmet

doi:10.1007/s00595-007-3614-5

Cited by 23 publications

(14 citation statements)

References 24 publications

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“…Administration of ALC and NAC during the first 24 hours has also been shown to reduce the volume of lesion after traumatic brain injury [45], [46]. Both antioxidants have in addition been tested as early neuroprotective treatments after ischemic spinal cord injury and provide significant reduction of motor dysfunction [47]–[49]. In the present study, we administered either NAC or ALC intrathecally for 4 weeks using osmotic minipumps and found marked neuroprotective effect on lesioned spinal motoneurons with almost complete restoration of density of dendritic branches and axonal terminals in the ventral horn.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of N-Acetyl-Cysteine and Acetyl-L-Carnitine after Spinal Cord Injury in Adult Rats

et al. 2012

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Following the initial acute stage of spinal cord injury, a cascade of cellular and inflammatory responses will lead to progressive secondary damage of the nerve tissue surrounding the primary injury site. The degeneration is manifested by loss of neurons and glial cells, demyelination and cyst formation. Injury to the mammalian spinal cord results in nearly complete failure of the severed axons to regenerate. We have previously demonstrated that the antioxidants N-acetyl-cysteine (NAC) and acetyl-L-carnitine (ALC) can attenuate retrograde neuronal degeneration after peripheral nerve and ventral root injury. The present study evaluates the effects of NAC and ALC on neuronal survival, axonal sprouting and glial cell reactions after spinal cord injury in adult rats. Tibial motoneurons in the spinal cord were pre-labeled with fluorescent tracer Fast Blue one week before lumbar L5 hemisection. Continuous intrathecal infusion of NAC (2.4 mg/day) or ALC (0.9 mg/day) was initiated immediately after spinal injury using Alzet 2002 osmotic minipumps. Neuroprotective effects of treatment were assessed by counting surviving motoneurons and by using quantitative immunohistochemistry and Western blotting for neuronal and glial cell markers 4 weeks after hemisection. Spinal cord injury induced significant loss of tibial motoneurons in L4–L6 segments. Neuronal degeneration was associated with decreased immunostaining for microtubular-associated protein-2 (MAP2) in dendritic branches, synaptophysin in presynaptic boutons and neurofilaments in nerve fibers. Immunostaining for the astroglial marker GFAP and microglial marker OX42 was increased. Treatment with NAC and ALC rescued approximately half of the motoneurons destined to die. In addition, antioxidants restored MAP2 and synaptophysin immunoreactivity. However, the perineuronal synaptophysin labeling was not recovered. Although both treatments promoted axonal sprouting, there was no effect on reactive astrocytes. In contrast, the microglial reaction was significantly attenuated. The results indicate a therapeutic potential for NAC and ALC in the early treatment of traumatic spinal cord injury.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of N-Acetyl-Cysteine and Acetyl-L-Carnitine after Spinal Cord Injury in Adult Rats

et al. 2012

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“…MDA is a metabolite of lipid peroxidase and it increases after spinal cord ischemia [25] . The levels of MDA demonstrate lipid peroxidation, which is thus considered to be evidence of reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Anti-Oxidative Effect of Lipoic Acid in Spinal Cord Ischemia/Reperfusion

et al. 2010

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Objective: Lipoic acid (LA) is an effective anti-oxidant agent that can scavenge free radicals in biological systems. The aim of this research was to study the probable protective effect of LA in spinal ischemic/reperfusion (I/R) injury. Materials and Methods: Thirty male Wistar rats, weighing 230–285 g, were assigned randomly into 3 groups (10 animals in each group): sham spinal I/R, and spinal I/R + LA. The spinal I/R + LA rats received LA 100 mg/kg subcutaneously 3 days prior to ischemia induction and 3 days after. The induction of ischemia lasted for 30 min. Results: At 72 h postoperatively, the neurological status was worse in the I/R group than the sham group (p < 0.05). The neurological status of animals in the LA-treated group appeared better than the I/R group (p < 0.05). In the I/R group, tissue glutathione peroxidase (GPx) and super oxide dismutase (SOD) activity were significantly less compared to the control group (p < 0.05). In the LA-treated group, tissue GPx and SOD levels were higher compared to the I/R group (p < 0.05). Conclusions: LA pretreatment reduced neurologic injury in the rats, most probably by maintaining the oxidant/anti-oxidant ion balance during spinal cord ischemia. Reperfusion may have contributed to the protective effects seen in the LA pretreatment.

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“…The most notable one is xanthine oxidase, which can directly reduce molecular oxygen to superoxide and hydrogen peroxide. 11 Antioxidant defenses. ROS participate in physiological processes, such as cell signaling.…”

Section: Ros and Oxidative Stress In Scimentioning

confidence: 99%

Oxidative stress in spinal cord injury and antioxidant-based intervention

Jia

Zhu

Li³

et al. 2011

Spinal Cord

259

176

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Study design: Literature review. Objectives: Spinal cord injury (SCI) remains a major public health issue in developed countries as well as worldwide. The pathophysiology of SCI is characterized by an initial primary injury followed by secondary deterioration. Although the etiology and pathogenesis of SCI remain to be fully understood, it has been suggested that reactive oxygen species (ROS) and oxidative stress have a significant role in the pathophysiology of SCI. Thus, alleviating oxidative stress may be an effective strategy for therapeutic intervention of SCI. The aim of this review was to describe (i) the sources of ROS as well as the major antioxidant defenses with particular attention being paid to lipid peroxidation; (ii) the biomarkers of oxidative stress in SCI and (iii) the neuroprotective effects of various compounds with antioxidative properties in animal models of SCI. Methods: PubMed, one of the most comprehensive biomedical databases, was searched from 1976-2011. All relevant papers were read by title, abstract and full-length article. Results: Oxidative stress is considered a hallmark of injury of SCI. Thus, alleviating oxidative stress may be an effective way of therapeutic intervention of SCI. Two of these agents, the glucocorticoid steroid methylprednisolone and the non-glucocorticoid 21-aminosteroid tirilazad, have been shown to possess significant antioxidant activities and improve recovery of SCI patients in clinical trials. Other promising botanical compounds and their molecular targets and mechanisms of action with regard to potential protection against SCI were also described. These include carotenoids and phenolic compounds. Conclusion: ROS and oxidative stress have a significant role in the pathophysiology of SCI. Alleviating oxidative stress is be an effective strategy for therapeutic intervention of SCI. Extensive research over the past several decades has identified numerous bioactive compounds that have antioxidative stress benefits in animal models of SCI. Thus, continued studies on bioactive compounds with ROS-scavenging capacity may lead to the development of effective antioxidant-based modalities for treating SCI in human subjects.

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Prevention of reperfusion injury of the spinal cord in aortic surgery: An experimental study

Abstract: We concluded that antioxidant agent combinations (diltiazem, N-acetylcysteine, and catalase) applied after ischemia might thus help protect the spinal cord against ischemia and reperfusion injury.

Cited by 23 publications

References 24 publications

Neuroprotective Effects of N-Acetyl-Cysteine and Acetyl-L-Carnitine after Spinal Cord Injury in Adult Rats

Neuroprotective Effects of N-Acetyl-Cysteine and Acetyl-L-Carnitine after Spinal Cord Injury in Adult Rats

Anti-Oxidative Effect of Lipoic Acid in Spinal Cord Ischemia/Reperfusion

Oxidative stress in spinal cord injury and antioxidant-based intervention

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