Hydrogen sulfide mediated protection against oxidative stress after spinal cord injury

Reactive oxygen species (ROS) and oxidative stress play a crucial role in pathophysiology of spinal cord injury (SCI). Recently, it has been suggested that hydrogen sulfide (H2S) is an effective agent for attenuation of a variety of pathophysiological processes. Up to now, the relationship between H...

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Bibliographic Details
Published inFolia neuropathologica Vol. 56; no. 3; p. 250
Main Authors Kisucka, A, Bimbova, K, Stropkovska, A, Bacova, M, Lukacova, N
Format Journal Article
LanguageEnglish
Published Warsaw Termedia sp. z o.o 01.01.2018
Subjects
Antioxidants
Apoptosis
Catalase
Compression
Data processing
Hydrogen peroxide
Hydrogen sulfide
Immunohistochemistry
Neurotoxicity
Oxidation
Oxidative stress
Reactive oxygen species
Spinal cord injuries
Superoxide dismutase
Surgery
Trauma
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Summary:Reactive oxygen species (ROS) and oxidative stress play a crucial role in pathophysiology of spinal cord injury (SCI). Recently, it has been suggested that hydrogen sulfide (H2S) is an effective agent for attenuation of a variety of pathophysiological processes. Up to now, the relationship between H2S and oxidative stress in spinal cord after trauma remains unknown. The aim of the present study was to explore the therapeutic potential of H2S against oxidative stress in rodent model of SCI. Adult Wistar rats were divided into three experimental groups: (1) control group, (2) Th9-compression (40 g/15 min) group, and (3) Th9-compression (40 g/15 min) + GYY4137. GYY4137, the slow-releasing H2S donor was applied in single dose (133 µmol/kg, i.p.) immediately after SCI. The animals survived 24 hours. The effect of H2S was examined by several parameters. The activity of antioxidant enzymes (superoxide dismutase, catalase) and the level of glutamate was measured 3 h, 6 h and 24 h after surgery in the blood serum, and the expression of neural markers was identified by real-time PCR and immunohistochemistry 24 h post-injury in Th8-Th10 segments. We have found significant increase of superoxide dismutase activity 6 h after the Th9 compression. Acute GYY4137 treatment markedly decreased the superoxide dismutase activity at 3 h and at 6 h, and considerably reduced the catalase activity in the blood serum 24 h post-injury. Immunohistochemical and PCR analyses indicated that early application of GYY4137 prevented the neurons from oxidative stress. This drug effectively reduced apoptosis, inflammation and glutamate neurotoxicity. Our data indicate that H2S scavenges superoxide early after SCI, while catalase exert its effect in scavenging the hydrogen peroxide in later post-SCI period. GYY4137, as a slow-releasing H2S compound is a potential therapeutic agent which could be used in treatment of SCI.
ISSN:1641-4640
1509-572X