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      Effects of individual or combined use of alpha-lipoic acid and methylprednisolone on malondialdehyde, superoxide dismutase, and catalase levels in acute spinal cord injury in rats

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          Abstract

          Introduction:

          Recent studies have demonstrated that alpha-lipoic acid (ALA) has a strong antioxidant property and it exerts neurotrophic effects on the peripheral nerves. In this study, we investigated potential effects of ALA on secondary injury mechanisms as well as on apoptosis.

          Methods:

          Forty Sprague-Dawley rats were equally divided into 5 groups, as follows: laminectomy (control), laminectomy + trauma (Trauma), laminectomy + posttraumatic methylprednisolone [MP] (Trauma + MP), laminectomy + posttraumatic ALA (Trauma + ALA), laminectomy + posttraumatic MP and ALA (Trauma + MP + ALA). Yasargil aneurysm clip method was used to induce the spinal cord injury. Twenty-four hours after the procedure the rats were sacrificed. Spinal cord samples were harvested to analyze malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels, as well as histopathological characteristics.

          Results:

          The Kruskal-Wallis test (95% confidence level, p < 0.05) showed a statistically significant difference between the groups in MDA ( p = 0.006), CAT ( p = 0.000), and SOD ( p = 0.001) levels. Pairwise comparisons, with Bonferroni correction, of control and Trauma group with the other groups, revealed a significant difference in CAT and SOD levels. Overall, our results showed that ALA administration significantly decreased MDA levels in Trauma + ALA compared to the same effect of MP in Trauma + MP group. Furthermore, ALA administration increased SOD and CAT levels in Trauma + ALA group. The combined use of ALA and MP demonstrated synergistic effects and yielded even more significant results.

          Conclusions:

          A combined use of ALA and MP might provide a benefit in patients exposed to spinal cord injury. However, at present, further studies are required to confirm these results.

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          Most cited references36

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          Degeneration and regeneration of axons in the lesioned spinal cord.

          For many decades, the inability of lesioned central neurons to regrow was accepted almost as a "law of nature", and on the clinical level, spinal cord and brain lesions were seen as being irreversible. Today we are starting to understand the mechanisms of neuronal regeneration in the central nervous system and its presence in the periphery. There is now a rapid expansion in this field of neuroscience. Developmental neurobiology has produced tools and concepts that start to show their impact on regeneration research. This is particularly true for the availability of antibodies and factors and for the rapidly growing cellular and molecular understanding of crucial aspects of neurite growth, guidance, target finding, and synapse stabilization. New cell biological concepts on the mechanisms of neuron survival and death and on the interaction of inflammatory cells with the central nervous system also find their way into the field of spinal cord and brain lesions and have, indeed, led already to new therapeutic approaches. This review briefly summarizes the current knowledge on the mechanisms involved in degeneration and tissue loss and in axonal regeneration subsequent to spinal cord lesions, particularly in mammals and humans.
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            Advances in secondary spinal cord injury: role of apoptosis.

            The outcome of spinal cord injury depends on the extent of secondary damage produced by a series of cellular and molecular events initiated by the primary trauma. This article reviews the evidence that secondary spinal cord injury involves the apoptotic as well as necrotic death of neurons and glial cells. Also discussed are the major factors that can contribute to cell death, such as glutamatergic excitotoxicity, free radical damage, cytokines, and inflammation. The development of innovative therapeutic strategies to reduce secondary spinal cord injury depends on an increased understanding of secondary injury mechanisms at the molecular and biochemical level. Such therapeutic interventions may include the use of antiapoptotic drugs, free radical scavengers, and anti-inflammatory agents. These could be targeted to block key reactions on cellular and molecular injury cascades, thus reducing secondary tissue damage, minimizing side effects, and improving functional recovery.
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              • Article: not found

              Effect of antioxidant treatment of streptozotocin-induced diabetic rats on endoneurial blood flow, motor nerve conduction velocity, and vascular reactivity of epineurial arterioles of the sciatic nerve.

              We have shown that diabetes-induced reduction in endoneurial blood flow (EBF) and impaired endothelium-dependent vascular relaxation precede slowing of motor nerve conduction velocity (MNCV) and decreased sciatic nerve Na(+)/K(+) ATPase activity. Furthermore, vascular dysfunction was accompanied by an accumulation of superoxide in arterioles that provide circulation to the sciatic nerve. In the present study, we examined the effect that treatment of streptozotocin-induced diabetic rats with antioxidants has on vascular and neural function. Diabetic rats were treated with 0.5% alpha-lipoic acid as a diet supplement or with hydroxyethyl starch deferoxamine (HES-DFO) by weekly intravenous injections at a dose of 75 mg/kg. The treatments significantly improved diabetes-induced decrease in EBF, acetylcholine-mediated vascular relaxation in arterioles that provide circulation to the region of the sciatic nerve, and MNCV. The treatments also reduced the production of superoxide by the aorta and superoxide and peroxynitrite by arterioles that provide circulation to the region of the sciatic nerve. Treating diabetic rats with alpha-lipoic acid prevented the diabetes-induced increase in thiobarbituric acid-reactive substances in serum and significantly improved lens glutathione levels. In contrast, treating diabetic rats with HES-DFO did not prevent diabetes-induced changes of either of these markers of oxidative stress. Diabetes-induced increase in sciatic nerve conjugated diene levels was not improved by treatment with either alpha-lipoic acid or HES-DFO. Treating diabetic rats with alpha-lipoic acid but not HES-DFO partially improved sciatic nerve Na(+)/K(+) ATPase activity and myo-inositol content. The increase in sciatic nerve sorbitol levels in diabetic rats was unchanged by either treatment. These studies suggest that diabetes-induced oxidative stress and the generation of superoxide may be partially responsible for the development of diabetic vascular and neural complications.
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                Author and article information

                Journal
                JHS
                Journal of Health Sciences
                University of Sarajevo Faculty of Health Studies (Bosnia )
                2232-7576
                1986-8049
                2016
                : 6
                : 3
                : 174-183
                Affiliations
                [1 ]Department of Neurosurgery, Kilis State Hospital, Kilis, Turkey
                [2 ]Department of Neurosurgery, Istanbul Bakirkoy Prof. Dr. Mazhar Osman Psychiatric Training and Research Hospital, Istanbul, Turkey
                [3 ]Department of Neurosurgery, Medipol University, Istanbul, Turkey
                [4 ]Department of Neurosurgery, Haseki Training and Research Hospital, Istanbul, Turkey
                [5 ]Department of Neurosurgery, Sisli Florence Nightingale Hospital, Istanbul Bilim University, Istanbul, Turkey
                Author notes
                [* ]Corresponding author: Gokhan Canaz, Department of Neurosurgery, Istanbul Bakirkoy Prof. Dr. Mazhar Osman Psychiatric Training and Research Hospital, Dr. Tevfik Sağlam Street No:25/2 Post Code: 34147 Bakirkoy/Istanbul. Phone: +90 212 409 15 15. E-mail: gokhancanaz@ 123456gmail.com
                Article
                JHS-6-174
                10.17532/jhsci.2016.409
                a936a720-82cd-4baf-929d-1d0e2d765a9d
                Copyright: © 2016 Alper Birgul et al.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 November 2016
                : 10 December 2016
                Categories
                RESEARCH ARTICLE

                Nursing,General medicine,Medicine,Molecular medicine,Life sciences
                malondialdehyde,Alpha-lipoic acid,spinal cord ınjury,methylprednisolone,superoxide dismutase

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