Methane Suppresses Microglial Activation Related to Oxidative, Inflammatory, and Apoptotic Injury during Spinal Cord Injury in Rats

Objective. We investigated the hypothesis that methane-rich saline (MS) can be used to repair spinal cord injury (SCI) in a rat model through suppressing microglial activation related to oxidative, inflammatory, and apoptotic injury. Methods. MS was injected intraperitoneally in rats after SCI. Hema...

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Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2017-01, Vol.2017 (2017), p.1-11
Main Authors: Ye, Xiaojian, Xie, Ning, Yu, Jiangming, Sun, Aijun, Li, Jian, Huang, Xiaodong, Wang, WeiHeng, Xi, Yanhai
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Care and treatment
Chromatography
Cytokines
Development and progression
Diabetic retinopathy
Disease Models, Animal
Female
Gases
Health aspects
Inflammation
Ischemia
Medical research
Membranes
Methane
Methane - pharmacology
Methane - therapeutic use
Microglia - metabolism
Natural gas utilities
Oxidative stress
Oxidative Stress - drug effects
Physiologic salines
Physiology
Rats
Rats, Sprague-Dawley
Rodents
Spinal cord injuries
Spinal Cord Injuries - drug therapy
Spinal Cord Injuries - pathology
Studies
Surgery
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Summary:Objective. We investigated the hypothesis that methane-rich saline (MS) can be used to repair spinal cord injury (SCI) in a rat model through suppressing microglial activation related to oxidative, inflammatory, and apoptotic injury. Methods. MS was injected intraperitoneally in rats after SCI. Hematoxylin-eosin (HE) staining, oxidative stress, inflammatory parameters, and cell apoptosis were detected 72 h after SCI to determine the optimal dose. Then, we investigated the protective mechanisms and the long-term effects of MS on SCI. HE and microglial activation were observed. Neurological function was evaluated by the Basso, Beattie, and Bresnahan (BBB) scale. Results. MS can significantly decrease infarct area and inhibit oxidative stress, inflammation, and cell apoptosis 72 h following SCI. The MS protective effect at a dose of 20 ml/kg was better. Moreover, MS can significantly suppress microglial activation related to oxidative and inflammatory injury after SCI and improve hind limb neurological function. Conclusion. MS could repair SCI and reduce the release of oxidative stress, inflammatory cytokines, and cell apoptosis produced by activated microglia. MS provides a novel and promising strategy for the treatment of SCI.
ISSN:1942-0900
1942-0994
DOI:10.1155/2017/2190897