Anti-apoptotic and neuroprotective effects of alpha-lipoic acid on spinal cord ischemia–reperfusion injury in rabbits

Emmez, Hakan; Yıldırım, Zühal; Kale, Aydemir; Tönge, Mehmet; Durdağ, Emre; Börcek, Alp Özgün; Uçankuş, Lortlar Neşe; Doğulu, Fikret; Kılıç, Nedret; Baykaner, M. Kemali

doi:10.1007/s00701-010-0703-9

Cited by 34 publications

(23 citation statements)

References 62 publications

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“…In addition, administration of alpha-lipoic acid significantly decreased these levels. Our study showed similar results with this study (17).…”

Section: █ Discussionsupporting

confidence: 83%

“…Corticosteroids, lazaroids, gangliosides, calcium channel blockers, free radical scavengers, magnesium, sodium channel blockers, cyclosporin A, opioid receptor antagonists, Nmethyl-D-aspartate (NMDA) receptor antagonists, and thyrotropin-releasing hormone have been shown to be effective in experimental SCI models. In-vivo and in-vitro neuroprotective effects of NMDA and non-NMDA receptor antagonists have been shown, however their clinical use is being limited by their major adverse effects (17).…”

Section: █ Discussionmentioning

confidence: 99%

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Effects of atorvastatin on experimental spinal cord ischemia-reperfusion injury in rabbits

Kardeş

Çivi²,

Tufan³

et al. 2016

Turkish Neurosurgery

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ABSTRACT(ROS), and lipid peroxidation (43). Studies have demonstrated increased glutamate release, activation of glutamate receptors and accumulation of calcium result in increased glutamate (3,21).Statins are a group of drugs that competitively inhibit the 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase, the first enzyme of the HMG-CoA reductase pathway. This inhibition impedes production of mevalonate, the next molecule in the cascade producing cholesterol. This action ultimately █ INTRODUCTION S pinal cord injury (SCI) is a mechanical insult followed by a secondary cascade of biologic events promoting permanent tissue damage. Excitotoxicity, oxidative stress and inflammatory response are the mediators of secondary injury, which is -theoretically-preventable (5,16). In the central nervous system (CNS), ischemic traumatic injury, cell loss and neuronal dysfunction, is thought to be the result of glutamatemediated excitotoxicity, formation of reactive oxygen species AIm: Extent of secondary injury is the determinant of tissue destruction and functional worsening after primary spinal cord injury (SCI). Data have accumulated on alleviation of secondary injury in SCI from many studies on the subject. Besides its cholesterol lowering effects, statins are known to have anti-inflammatory and anti-oxidant effects which are the main targets of spinal cord research. This study aims to evaluate the effects of atorvastatin on experimental spinal cord ischemia-reperfusion injury. mATERIAl and mEThODS: Thirty adult male New Zealand rabbits were allocated into control, ischemia-reperfusion (I/R) and treatment groups. Treatment group received 5 mg/kg of atorvastatin via lavage for the preceding 14 days. Other groups received placebo during the same time period. After two weeks, animals in the I/R and treatment groups underwent abdominal temporary aorta occlusion for 30 minutes. Neurological condition of the animals was recorded during the 48 hours of observation. Afterwards, animals were sacrificed and levels of malondialdehyde, glutathione and nitric oxide in spinal cord tissue and plasma and the histopathological tissue changes were determined. RESUlTS:Animals in the treatment groups demonstrated significantly better results than the I/R group regarding biochemical markers. Neurological evaluation using the Tarlov scale demonstrated significantly better results at the 48 th hour in treatment group. Histopathological results were also better in the treatment groups. CONClUSION:Results of this study demonstrate the neuroprotective effects of atorvastatin. Atorvastatin has favorable effects on biochemical markers of oxidative stress in SCI. Further studies with larger cohorts and different time periods are also needed.

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“…In addition, administration of alpha-lipoic acid significantly decreased these levels. Our study showed similar results with this study (17).…”

Section: █ Discussionsupporting

confidence: 83%

Section: █ Discussionmentioning

confidence: 99%

Effects of atorvastatin on experimental spinal cord ischemia-reperfusion injury in rabbits

Kardeş

Çivi²,

Tufan³

et al. 2016

Turkish Neurosurgery

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“…Moreover, because of its amphiphilic nature, ALA readily penetrates all cells and tissues of the body, including the bloodbrain barrier (BBB). ALA also effectively increases the production of acetylcholine (neurotransmitter) and thereby maintains the integrity of the brain [12]. These findings strongly suggest a role for ALA in the treatment of various neurological disorders.…”

Section: Introductionmentioning

confidence: 77%

“…ALA administration, especially 100 vs. 50 mg, significantly reduced LPO levels to near normal. Emmez and coworkers [12] showed that ALA, with its freeradical scavenging activity, significantly suppressed LPO.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of α-lipoic acid against hypoxic– ischemic brain injury in neonatal rats

Mei¹,

Yang²

2017

Trop. J. Pharm Res

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“…The pathophysiologic mechanisms that underlie hypoxic/ischemic injury to the spinal cord have not been totally explained yet. [1][2][3][4][5][6][7] Thoracic and thoracoabdominal aortic intervention carries a significant risk of spinal cord ischemia, ranging from 5 to 20%. [8][9][10] Pouw et al 11 compared the neurological outcome between paraplegia caused by acute spinal cord ischemia syndrome and traumatic SCI, and found that neurological outcome was independent of the diagnosis.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical analysis of TIMP-2 and collagen types I and IV in experimental spinal cord ischemia–reperfusion injury in rats

Anık

Köktürk

Genç

et al. 2011

The Journal of Spinal Cord Medicine

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Background: Thoracic and thoracoabdominal aortic intervention carries a significant risk of spinal cord ischemia. The pathophysiologic mechanisms that cause hypoxic/ischemic injury to the spinal cord have not been totally explained. In normal spinal cord, neurons and glial cells do not express type IV collagen. Type IV collagen produced by reactive astrocytes is reported to participate in glial scar formation. Tissue inhibitors of metalloproteinases (TIMPs) are endogenous inhibitors that regulate the activity of the matrix metalloproteinases (MMPs). TIMP-2 binds strongly with MMP-2, facilitating activation by membrane-type MMP. Imbalance between TIMPs and MMPs can lead to excessive degradation of matrix components. Type IV collagen involved in the blood-brain barrier disruption and glial scar formation, TIMP-2 influences MMP-2 that controls degradation of collagen I and IV. Objective: To examine the immunohistochemical analysis of TIMP-2 and collagen types I-IV in experimental spinal cord ischemia-reperfusion in rats. Methods: Thirty-two male Wistar rats weighing 250-300 g were divided into four groups: group S: sham group (n = 8); group 0P: 30-minute occlusion without perfusion (n = 8); group 3P: 30-minute occlusion and 3-hour perfusion (n = 8); and group 24P: 30-minute occlusion and 24-hour perfusion (n = 8). Infrarenal aorta was cross-clamped at two sites by using two aneurysm clips for 30 minutes. Reperfusion was provided after removal of the clips. Lumbar spinal cord segments were removed for immunohistochemical analysis. Results: TIMP-2 and collagen staining in 3-hour perfused (3P) group were nearly the same with sham group (S). TIMP-2 and collagen staining increased in the 24-hour perfused group. Conclusion: Alterations in collagen levels may relate to the biphasic breakdown of the blood-brain barrier and collagen staining in new cell types with relation to glial scar formation. Our results demonstrate that 3-hour perfusion after occlusion in hypoxic/ischemic spinal cord injury seems to be the critical reversible period.

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Anti-apoptotic and neuroprotective effects of alpha-lipoic acid on spinal cord ischemia–reperfusion injury in rabbits

Abstract: Although further studies considering different dose regimens and time intervals are required, the results of the present study prove that alpha-lipoic acid has favorable effects on experimental spinal cord ischemia-reperfusion injury.

Cited by 34 publications

References 62 publications

Effects of atorvastatin on experimental spinal cord ischemia-reperfusion injury in rabbits

Effects of atorvastatin on experimental spinal cord ischemia-reperfusion injury in rabbits

Neuroprotective effects of α-lipoic acid against hypoxic– ischemic brain injury in neonatal rats

Immunohistochemical analysis of TIMP-2 and collagen types I and IV in experimental spinal cord ischemia–reperfusion injury in rats

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