Neuroprotective effects of testosterone on ischemia/reperfusion injury of the rabbit spinal cord

Gürer, Bora; Kertmen, Hayri; Kasim, Emin; Yı́lmaz, Erdal; Kanat, Burhan Hakan; Sargon, Mustafa F.; Arıkök, Ata Türker; Ergüder, Berrin İmge; Şekerci, Zeki

doi:10.1016/j.injury.2014.11.002

Cited by 53 publications

(51 citation statements)

References 54 publications

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“…The present study demonstrated that lipid peroxidation was significantly increased 24 h after ischemia/reperfusion, whereas SOD1 activity was decreased. This result was supported by previous studies, which demonstrated that spinal cord ischemia increases lipid peroxidation and the subsequent inactivation and consumption of SOD1 in the spinal cord (38)(39)(40). A previous study reported that at H 2 O 2 concentrations of 1 mM and below, SUMO-1, -2, and -3 conjugates were almost completely lost (37).…”

Section: Discussionsupporting

confidence: 84%

SUMO-1 delays neuronal damage in the spinal cord following ischemia/reperfusion

Jung

Kim

Kwon

et al. 2017

Molecular Medicine Reports

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The present study investigated the protective effects of small ubiquitin-like modifier 1 (SUMO-1) on spinal cord ischemic damage in rabbits. A trans‑activator of transcription (Tat)‑SUMO‑1 fusion protein was prepared, and transient spinal cord ischemia was induced by occlusion of the abdominal aorta for 15 min. Vehicle (glycerol) or 1 mg/kg Tat-1-SUMO‑1 was administered intraperitoneally to the rabbits immediately following ischemia/reperfusion. Administration of Tat-SUMO-1 did not lead to significant alterations in arterial blood gases [partial pressure (Pa)CO2 and PaO2], pH, or blood glucose levels prior to ischemia, 10 min after occlusion or 10 min after reperfusion. Mean arterial pressure was significantly decreased only during occlusion. Motor behaviors were assessed at 24, 48 and 72 h after ischemia/reperfusion using Tarlov's criteria. Administration of Tat‑SUMO‑1 significantly improved Tarlov scores 24 h after ischemia/reperfusion and the number of cresyl violet positive neurons was significantly increased in the ventral horn of the spinal cord compared with the vehicle‑treated group. However, Tarlov scores were consistently decreased at 48 and 72 h after ischemia/reperfusion in the Tat‑SUMO‑1‑treated group, and Tarlov scores and the number of cresyl violet positive neurons were not significantly different between the vehicle‑ and Tat‑SUMO‑1‑treated groups after 72 h. Tat-SUMO‑1 administration significantly ameliorated a reduction in Cu, Zn‑superoxide dismutase activity and an increase in lipid peroxidation 24 h after ischemia/reperfusion; however, these effects were not present at 72 h. These results suggested that Tat‑SUMO‑1 may delay, although not protect against, neuronal death by regulating oxidative stress in the ventral horn of the spinal cord and that combination therapy using Tat‑SUMO‑1 with other compounds may provide a therapeutic approach to decrease neuronal damage.

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Section: Discussionsupporting

confidence: 84%

SUMO-1 delays neuronal damage in the spinal cord following ischemia/reperfusion

Jung

Kim

Kwon

et al. 2017

Molecular Medicine Reports

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“…Most important mechanisms that lead to neuronal damage after spinal cord I/R injury appear to be hypoxia with energy failure, excitotoxicity, oxidative stress, inflammation, lipid peroxidation, and apoptosis. 11 Neuronal cell is comparatively sensitive to hypoxia resulted from ischemia and then subjects to cell apoptosis, which is supposed to the major cause of neuron death. In the present study, we also found that the amount of apoptotic cells in the neuronal cells exposed to hypoxia was significantly elevated than the cells in normoxic conditions.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia promotes apoptosis of neuronal cells through hypoxia-inducible factor-1α-microRNA-204-B-cell lymphoma-2 pathway

Wang

et al. 2015

Exp Biol Med (Maywood)

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Neuronal cells are highly sensitive to hypoxia and may be subjected to apoptosis when exposed to hypoxia. Several apoptosisrelated genes and miRNAs involve in hypoxia-induced apoptosis. This study aimed to examine the role of HIF1a-miR-204-BCL-2 pathway in hypoxia-induced apoptosis in neuronal cells. Annexin V/propidium iodide assay was performed to analyze cell apoptosis in AGE1.HN and PC12 cells under hypoxic or normoxic conditions. The expression of BCL-2 and miR-204 were determined by Western blot and qRT-PCR. The effects of miR-204 overexpression or knockdown on the expression of BCL-2 were evaluated by luciferase assay and Western blot under hypoxic or normoxic conditions. HIF-1a inhibitor YC-1 and siHIF-1a were employed to determine the effect of HIF-1a on the up-regulation of miR-204 and down-regulation of BCL-2 induced by hypoxia. Apoptosis assay showed the presence of apoptosis induced by hypoxia in neuronal cells. Moreover, we found that hypoxia significantly down-regulated the expression of BCL-2, and increased the mRNA level of miR-204 in neuronal cells than that in control. Bioinformatic analysis and luciferase reporter assay demonstrated that miR-204 directly targeted and regulated the expression of BCL-2. Specifically, the expression of BCL-2 was inhibited by miR-204 mimic and enhanced by miR-204 inhibitor. Furthermore, we detected that hypoxia induced cell apoptosis via HIF-1a/miR-204/BCL-2 in neuronal cells. This study demonstrated that HIF-1a-miR-204-BCL-2 pathway contributed to apoptosis of neuronal cells induced by hypoxia, which could potentially be exploited to prevent spinal cord ischemia-reperfusion injury.

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“…The housing facility maintained national standards, in compliance with the Laboratory Animal-Requirements of Environment and Housing Facilities (GB 14925-2001) [8]. The rabbits in the groups with low Tarlov scores [9]were maintained on the premises with su cient water and food under standard animal housing conditions. They could feed themselves with the help of an animal administrator.…”

Section: Perioperative Managementmentioning

confidence: 99%

WITHDRAWN: Changes of the F-wave in the acute phase of permanent spinal cord ischaemic injury predict spinal cord function in animal models of rabbits

Zhou

Liu

Heng

et al. 2020

Preprint

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Background ：To explore the changes of the F-wave in the posterior tibial nerve of rabbits after different levels of lumbar spinal cord ischaemic injury and its correlation with motor function and the extent of lumbar spinal cord pathological damage. Methods ： Thirty New Zealand rabbits were randomly divided into 6 groups. The control group (n=5) was used to exclude the influence of anaesthesia and surgery on the F-wave. Different levels of lumbar arteries were ligated in the five experimental groups (n=5). The F-wave was recorded to observe the changes in the acute phase of spinal cord ischaemia.The correlation between the changes of the F-wave in the acute reversible phase and the motor function of the spinal cord was analysed. Results ： The results for the control group indicated that anaesthesia and surgery did not affect the F-wave results.There was no statistically significant difference in the F-wave amplitudes and latency before and after ligation in the 1 and 2 level ligation groups. The F-wave changed immediately after ligation in the 3, 4 and 5 ligation groups. The latency of the F-wave gradually extended, the amplitude of the F-wave gradually reduced.The amplitude variations of the F-wave were positively correlated with the motor function 2 days after ligation, there was a statistically significant difference. Conclusion ：The F-waves in the posterior tibial nerve of rabbits were found to be sensitive to the lumbar spinal cord ischaemic injury and specific to predict motor function.

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Neuroprotective effects of testosterone on ischemia/reperfusion injury of the rabbit spinal cord

Cited by 53 publications

References 54 publications

SUMO-1 delays neuronal damage in the spinal cord following ischemia/reperfusion

SUMO-1 delays neuronal damage in the spinal cord following ischemia/reperfusion

Hypoxia promotes apoptosis of neuronal cells through hypoxia-inducible factor-1α-microRNA-204-B-cell lymphoma-2 pathway

WITHDRAWN: Changes of the F-wave in the acute phase of permanent spinal cord ischaemic injury predict spinal cord function in animal models of rabbits

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