The efficacy of antioxidants in functional recovery of spinal cord injured rats: an experimental study

Robert, Asirvatham Alwin; Zamzami, Marwan; Sam, Asirvatham Edwin; Jadid, Maher Al; Mubarak, Sultan Al

doi:10.1007/s10072-011-0829-4

Cited by 23 publications

(12 citation statements)

References 25 publications

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“…These findings are consistent with a role of vitamin E in enhancing nerve conductivity in the injured cord which is may also explain the significant increase in the BBB locomotion scores seen in these animals fed with the enriched vitamin E diet reported here. These data expand previous work showing vitamin E improving locomotion when administered in a prophylactic manner [ 43 , 44 , 48 ] or after injury [ 45 , 46 ]. When compared to vitamin C supplementation after injury, vitamin E was shown to be more effective for locomotion recovery [ 46 ].…”

Section: Discussionsupporting

confidence: 88%

“…Further, dietary vitamin E for 8 weeks before SCI decreased reactive oxygen species (ROS) while improved locomotion, blood flow and spinal cord evoked potentials, and decreased ROS in rats [ 44 ]. While these studies did not use the standardized scale to measure locomotion after SCI, the Basso, Beattie, and Bresnahan (BBB) scale, their findings provided support for a promising neuroprotective role of vitamin E. Further, dietary vitamin E supplementation for 14 days after injury was shown to improve BBB scores [ 45 , 46 ] potentially involving the inhibition of lipid peroxidation products such as thiobarbituric acid reactive substances and malondialdehyde [ 44 , 47 , 48 ]. Thus, prior studies suggest a neuroprotective role of vitamin E during SCI, but little is known about potential targets, primary cellular processes involved and whether it can affect other primary functions affected by SCI.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Dietary Vitamin E Supplementation in Bladder Function and Spasticity during Spinal Cord Injury

et al. 2018

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Traumatic spinal cord injury (SCI) results in debilitating autonomic dysfunctions, paralysis and significant sensorimotor impairments. A key component of SCI is the generation of free radicals that contributes to the high levels of oxidative stress observed. This study investigates whether dietary supplementation with the antioxidant vitamin E (alpha-tocopherol) improves functional recovery after SCI. Female adult Sprague-Dawley rats were fed either with a normal diet or a dietary regiment supplemented with vitamin E (51 IU/g) for eight weeks. The rats were subsequently exposed either to a contusive SCI or sham operation, and evaluated using standard functional behavior analysis. We report that the rats that consumed the vitamin E-enriched diet showed an accelerated bladder recovery and significant improvements in locomotor function relative to controls, as determined by residual volumes and Basso, Beatie, and Bresnaham BBB scores, respectively. Interestingly, the prophylactic dietary intervention did not preserve neurons in the ventral horn of injured rats, but it significantly increased the numbers of oligodendrocytes. Vitamin E supplementation attenuated the depression of the H-reflex (a typical functional consequence of SCI) while increasing the levels of supraspinal serotonin immunoreactivity. Our findings support the potential complementary use of vitamin E to ameliorate sensory and autonomic dysfunctions associated with spinal cord injury, and identified promising new cellular and functional targets of its neuroprotective effects.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Effects of Dietary Vitamin E Supplementation in Bladder Function and Spasticity during Spinal Cord Injury

et al. 2018

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“…[ [108][109][110][111][112] Vitamin C Stops lipid hydroperoxyides formation and decreases membrane damage.…”

Section: Neuroprotection Mechanismmentioning

confidence: 99%

Trends in Neuroprotective Strategies after Spinal Cord Injury: State of the Art

Rodríguez-Barrera¹,

Garibay-López²,

Ibarra³

2020

Neuroprotection - New Approaches and Prospects

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Spinal cord injury (SCI) is an important pathology leading to possibly fatal consequences. The most common repercussions are those affecting motor and sensitivity skills. SCI-damage occurs in its first phase-as a result of the lesion mechanism (contusion, compression, transection, and primary lesion). After this primary damage, there is a second phase with further deleterious effects on neural degeneration and tissue restoration. At the moment, several investigation groups are working on developing therapeutic strategies to induce neuroprotection. This chapter pretends to introduce the reader to a wide range of these therapies, particularly those with promising results and tested in preclinical and clinical studies. In the first section, physiopathology of SCI will be addressed. Afterwards, the chapter will review neuroprotective strategies such as cyclooxygenase, calpain, and apoptosis inhibitors. Finally, the effect of immunophilin ligands, neural-derived peptides, antioxidants, hypoglycemic agent, gonadal hormones, Na channel blockers, and transplant of cultured cells will also be reviewed.

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“…Since the complex molecular mechanisms of SCI have only been partially elucidated, most efforts so far have had limited efficacy. These efforts mainly involve providing anti-neuro-inflammatory conditions [30,[35][36][37] preventing excitotoxicity in neurons [38,39] , reducing oxidative damage [31,40,41] and regulating the effects of intracellular ionic changes, such as altered Ca 2+ homeostasis.…”

Section: Current Studies For the Recovery Of Scimentioning

confidence: 99%

Speedy/RINGO: a molecular savior in spinal cord injury-based neurodegeneration?

Kaya¹,

Yıldız²

2019

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Endogenous or exogenous insults can cause spinal cord injury (SCI), often resulting in the loss of motor, autonomic, sensory and reflex functions. The pathogenesis of SCI comprises two stages. The primary injury stage occurs at the moment of trauma and is characterized by hemorrhage and rapid cell death. The secondary injury stage occurs due to progression of primary damage and is characterized by tissue loss and functional disorder. One of the most important cellular mechanisms underlying secondary injury is glutamate excitotoxicity, which overactivates the calpain protease via excessive Ca 2+ influx and induces neuronal apoptosis via p53 induction. Furthermore, Ca 2+ influx elicits apoptosis by inducing p53, thus negatively affecting two pathways: the mitogenic extracellular signal-regulated kinase/mitogenactivated protein kinase (ERK/MAPK) pathway and the survival phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway. Speedy/rapid inducer of G2/M progression in oocytes (Speedy/RINGO) is a cell cycle regulatory protein that increases survival of p53-positive mitotic cells by inhibiting the apoptotic machinery. Moreover, this protein elicits p53dependent anti-apoptotic effects on calpain-induced degeneration of primary hippocampal neurons, amyotrophic lateral sclerosis motor neurons, and astrocytes and microglia in spinal cord lesions. The pathophysiology of SCI has not been fully elucidated and this hinders the development of powerful therapeutic strategies. This review focuses on the cellular mechanisms underlying the anti-apoptotic effects of Speedy/RINGO and discusses how this protective function can possibly be exploited to facilitate recovery from SCI. Particular attention is paid to reversal of the negative effects on the ERK/MAPK and PI3K/AKT pathways via induction of p53.

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The efficacy of antioxidants in functional recovery of spinal cord injured rats: an experimental study

Cited by 23 publications

References 25 publications

Effects of Dietary Vitamin E Supplementation in Bladder Function and Spasticity during Spinal Cord Injury

Effects of Dietary Vitamin E Supplementation in Bladder Function and Spasticity during Spinal Cord Injury

Trends in Neuroprotective Strategies after Spinal Cord Injury: State of the Art

Speedy/RINGO: a molecular savior in spinal cord injury-based neurodegeneration?

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