Erythropoietin improves oxidative stress following spinal cord trauma in rats

Yazıhan, Nuray; Uzuner, Kubi̇lay; Salman, Bülent; Vural, Murat; Köken, Tülay; Arslantaş, Ali

doi:10.1016/j.injury.2008.03.010

Cited by 43 publications

(24 citation statements)

References 19 publications

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“…Secondary injury after the primary impact includes different pathophysiological and biochemical events. [3][4][5][6][7][8][9][10][11][12][13] Oxygen-derived free radicals have been implicated in the pathogenesis of spinal cord neuronal injury after trauma. Decreasing the level of oxidative stress minimizes the secondary destruction effect after traumatic injury.…”

Section: Resultsmentioning

confidence: 99%

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Antioxidant effects of curcumin in spinal cord injury in rats

Kavakli

Koca²,

Alıcı³

2011

Ulus Travma Acil Cerrahi Derg

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AMAÇBu deneysel çalışma, sıçanlarda spinal kord yaralanmasın-da curcuminin antioksidan etki yoluyla faydasını araştır-mak için yapıldı. GEREÇ VE YÖNTEMYirmi dört adet Wistar albino sıçan 3 gruba randomize edildi. Spinal kord yaralanması ağırlık düşürme modeliyle gerçekleştirildi. Grup 1'e laminektomi ardından spinal kord yaralanması uygulandı ve herhangi bir tedavi verilmedi. Grup 2'ye laminektomi ardından spinal kord yaralanması uygulandı ve curcumin verildi (200 mg/kg/gün ağızdan). Grup 3'e laminektomi ardından spinal kord yaralanması uygulandı ve metilprednizolon verildi (30 mg/kg periton içine), 24 saat sonra tüm sıçanlardan kan örnekleri alındı, sonra serum süperoksit dismutaz (SOD) ve malondialdehit (MDA) düzeyleri belirlendi ve elde edilen sonuçlar karşılaştırıldı. BULGULARCurcumin grubunda SOD düzeyi kontrol ve metilprednizolon grubundan daha yüksekti (p<0,001 ve p<0,012). Curcumin grubunda MDA düzeyi kontrol grubundan daha düşüktü (p<0,042). Benzer şekilde metilprednizolon grubunda MDA düzeyi kontrol grubundan daha düşüktü (p<0,001). SONUÇBu çalışmanın sonuçları curcuminin etkin biçimde oksidatif hasara karşı spinal kord dokularını koruduğunu gös-terir.Anahtar Sözcükler: Antioksidan; curcumin; malondialdehit; spinal kord yaralanması; süperoksit dismutaz.

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Section: Resultsmentioning

confidence: 99%

“…Decreasing the level of oxidative stress minimizes the secondary destruction effect after traumatic injury. [10] Methylprednisolone is a pharmacological agent that has clinically proven useful effects on functional recovery following SCI. [3,4] Additionally, curcumin has been shown to have various clinical and experimental beneficial effects.…”

Section: Resultsmentioning

confidence: 99%

Antioxidant effects of curcumin in spinal cord injury in rats

Kavakli

Koca²,

Alıcı³

2011

Ulus Travma Acil Cerrahi Derg

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“…These include methylene blue [110], mexilitine [111], thiopental [112], β-glucan [113], N-acetylcysteine [114], γ-glutamylcysteine [18], polyethylene glycol [115], edaravone (MCI186), cyclosporine A [116], NIM811 [117,118], erythropoietin [119] and α-lipoic acid [120]. Although some of these are probably true chemical antioxidants (e.g., methylene blue, edaravone, α-lipoic acid), others may work indirectly by induction of endogenous antioxidant defenses (e.g., N-acetylcysteine, γ-glutamylcysteine), reduction of mitochondrial dysfunction, and its associated free radical leakage (e.g., cyclosporine A, NIM811) or by enhancement of cell membrane repair mechanisms (e.g., polyethylene glycol).…”

Section: Efficacy Of Miscellaneous Antioxidants In Sci Modelsmentioning

confidence: 99%

Antioxidant Therapies for Acute Spinal Cord Injury

2011

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Summary:One of the most investigated molecular mechanisms involved in the secondary pathophysiology of acute spinal cord injury (SCI) is free radical-induced, iron-catalyzed lipid peroxidation (LP) and protein oxidative/nitrative damage to spinal neurons, glia, and microvascular cells. The reactive nitrogen species peroxynitrite and its highly reactive free radicals are key initiators of LP and protein nitration in the injured spinal cord, the biochemistry, and pathophysiology of which are first of all reviewed in this article. This is followed by a presentation of the antioxidant mechanistic approaches and pharmacological compounds that have been shown to have neuroprotective properties in preclinical SCI models. Two of these, which act by inhibition of LP, are high-dose treatment with the glucocorticoid steroid methylprednisolone (MP) and the nonglucocorticoid 21-aminosteroid tirilazad, have been demonstrated in the multicenter NASCIS clinical trials to produce at least a modest improvement in neurological recovery when administered within the first 8 hours after SCI. Although these results have provided considerable validation of oxidative damage as a clinically practical neuroprotective target, there is a need for the discovery of safer and more effective antioxidant compounds for acute SCI.

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“…[25,26] Similar efficiency has been reported in decreasing oxidative stress related to SCI. [27] Neuroprotection mechanism of tadalafil is not yet known; neurogenesis, synaptic plasticity, and physiological modulation of neurotransmitters caused by cGMP have all been proposed. [28][29][30][31] Most likely, tadalafil plays role in neuroprotection through effect on cGMP.…”

Section: Discussionmentioning

confidence: 99%