Acute 17β-Estradiol Pretreatment Protects Against Abdominal Aortic Occlusion Induced Spinal Cord Ischemic-Reperfusion Injury

Khalaj, Leila; Peirovi, Habibollah; Khodagholi, Fariba; Abdi, Azadeh; Dargahi, Leila; Ahmadiani, Abolhassan

doi:10.1007/s11064-010-0314-0

Cited by 12 publications

(8 citation statements)

References 59 publications

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“…In our present study, spinal cord ischemia significantly decreased the SOD and catalase levels in the spinal cord at 72 h after I-R. This result is consistent with previous studies that showed that I-R injury in the rabbit spinal cord significantly decreased the activities of SOD and catalase at 48 [35] and 72 h [21] post-ischemia. However, some experiments showed that SOD and CAT activities in the ischemic spinal cord were induced in response to I-R injury [34,36].…”

Section: Discussionsupporting

confidence: 93%

Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord

Kim

Yoo

et al. 2011

Neurochem Res

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A rabbit model of spinal cord ischemia has been introduced as a good model to investigate the pathophysiology of ischemia-reperfusion (I-R)-induced paraplegia. In the present study, we observed the effects of Cu,Zn-superoxide dismutase (SOD1) against ischemic damage in the ventral horn of L(5-6) levels in the rabbit spinal cord. For this study, the expression vector PEP-1 was constructed, and this vector was fused with SOD1 to create a PEP-1-SOD1 fusion protein that easily penetrated the blood-brain barrier. Spinal cord ischemia was induced by transient occlusion of the abdominal aorta for 15 min. PEP-1-SOD1 (0.5 mg/kg) was intraperitoneally administered to rabbits 30 min before ischemic surgery. The administration of PEP-1-SOD1 significantly improved neurological scores compared to those in the PEP-1 (vehicle)-treated ischemia group. Also, in this group, the number of cresyl violet-positive cells at 72 h after I-R was much higher than that in the vehicle-treated ischemia group. Malondialdehyde levels were significantly decreased in the ischemic spinal cord of the PEP-1-SOD1-treated ischemia group compared to those in the vehicle-treated ischemia group. In contrast, the administration of PEP-1-SOD1 significantly ameliorated the ischemia-induced reduction of SOD and catalase levels in the ischemic spinal cord. These results suggest that PEP-1-SOD1 protects neurons from spinal ischemic damage by decreasing lipid peroxidation and maintaining SOD and catalase levels in the ischemic rabbit spinal cord.

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Section: Discussionsupporting

confidence: 93%

Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord

Kim

Yoo

et al. 2011

Neurochem Res

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“…23 Some patients experience acute spinal cord dysfunction following thoracic aortic occlusion as a result of acute spinal cord ischemia from hypoperfusion during crossclamping. 16 In the English literature, the protective potential of curcumin has not yet been investigated in spinal cord ischemia-reperfusion injury induced by abdominal aortic occlusion. The aim of this study was to evaluate the Effects of curcumin on acute spinal cord ischemia-reperfusion injury in rabbits neuroprotective effects of curcumin on the acute phase of spinal cord ischemia-reperfusion injury.…”

mentioning

confidence: 99%

Effects of curcumin on acute spinal cord ischemia-reperfusion injury in rabbits

Kurt

Yıldırım²,

Cemil

et al. 2014

SPI

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Object. The object of this study was to conduct a prospective, randomized, laboratory investigation of the neuroprotective effects of curcumin functionally, biochemically, and histologically in an experimental acute spinal cord ischemia-reperfusion injury on rabbits.Methods. Eighteen rabbits were randomly assigned to 1 of 3 groups: the sham group, the ischemia-reperfusion group, or the curcumin group. Spinal cord ischemia was induced by applying an infrarenal aortic cross-clamp for 30 minutes. At 48 hours after ischemia, neurological function was evaluated with modified Tarlov criteria. Biochemical changes in the spinal cord and plasma were observed by measuring levels of malondialdehyde (MDA), advanced oxidation protein products (AOPP), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitrite/nitrate, and tumor necrosis factor-a (TNF-a). Histological changes were examined with H & E staining. Immunohistochemical staining with antibodies against caspase-3 was performed to evaluate cell apoptosis after ischemia.Results. In the curcumin group, neurological outcome scores were statistically significantly better compared with the ischemia-reperfusion group. In the ischemia-reperfusion group, MDA, AOPP, and nitrite/nitrate levels were significantly elevated in the spinal cord tissue and the plasma by the induction of ischemia-reperfusion. The curcumin treatment significantly prevented the ischemia-reperfusion-induced elevation of nitrite/nitrate and TNF-a. In addition, the spinal cord tissue and the plasma SOD, GSH, and CAT levels were found to be preserved in the curcumin group and not statistically different from those of the sham group. Histological evaluation of the tissues also demonstrated a decrease in axonal damage, neuronal degeneration, and glial cell infiltration after curcumin administration.Conclusions. Although further studies including different dose regimens and time intervals are required, curcumin could attenuate a spinal cord ischemia-reperfusion injury in rabbits via reducing oxidative products and proinflammatory cytokines, as well as increasing activities of antioxidant enzymes and preventing apoptotic cell death. (http://thejns.org/doi/abs/10.3171/2013 keY WorDs • antioxidant • curcumin • ischemia-reperfusion injury • neuroprotection • oxidative stress • spinal cord injuryAbbreviations used in this paper: AOPP = advanced oxidation protein products; CAT = catalase; GSH = glutathione; MDA = malondialdehyde; SOD = superoxide dismutase; TBARS = thiobarbituric acid reactive substances; TNF = tumor necrosis factor.

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“…Activation of caspase-3 is considered to be a reliable marker for apoptotic cell death [1][2][3][4][5] and is also involved in differentiation of neural and hematopoietic cells [6,7]. In the motor neuron cell line of the spinal cord, the treatment of caspase-3 inhibitor attenuates the toxicity of multi-catalytic proteasome inhibitor lactacystin [8].…”

Section: Introductionmentioning

confidence: 99%

Increased Immunoreactivities of Cleaved αII-Spectrin and Cleaved Caspase-3 in the Aged Dog Spinal Cord

et al. 2011

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The activation of caspase-3 is considered to be a reliable marker for apoptotic cell death, and a 120-kDa fragment of αII-spectrin is generated by caspase-3 mediated cleavage of this structural protein. In the present study, we compared cleaved αII-spectrin (120-kDa) and cleaved caspase-3-immunoreactive cells and their protein levels in the cervical (C₅-C₆) and lumbar (L₃-L₄) levels of the spinal cord in adult (1-2 year-old) and aged (10-12 year-old) dogs (German shepherds). Weak cleaved αII-spectrin and cleaved caspase-3 immunoreactivity was found in neurons of the adult group; however, their immunoreactivity was distinctively increased in the neuronal cytoplasm in the aged group compared to those in the adult group, although the distribution pattern of their neurons was similar between the adult and age group. In addition, cleaved αII-spectrin and cleaved caspase-3 levels in the aged spinal cord were markedly increased compared to those in the adult group. These findings suggest that the increases of cleaved αII-spectrin and cleaved caspase-3 immunoreactivity may be related to aging of the spinal cord in dogs.

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Acute 17β-Estradiol Pretreatment Protects Against Abdominal Aortic Occlusion Induced Spinal Cord Ischemic-Reperfusion Injury

Cited by 12 publications

References 59 publications

Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord

Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord

Effects of curcumin on acute spinal cord ischemia-reperfusion injury in rabbits

Increased Immunoreactivities of Cleaved αII-Spectrin and Cleaved Caspase-3 in the Aged Dog Spinal Cord

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