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

Abstract

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.

Therapeutic Hypothermia Improves Hind Limb Motor Outcome and Attenuates Oxidative Stress and Neuronal Damage in the Lumbar Spinal Cord Following Cardiac Arrest

“…Pathological changes between CA and ROSC may be related to the degree of neurological dysfunction. Microglia, resident immune cells in the central nervous system (CNS), are increased in number and morphologically activated at an early stage after spinal cord injury [35,36], which contributes to neuroinflammation and onset of neuronal damage by releasing large amount of inflammatory cytokines and ROS [37,38]. Similar to previous studies, our results showed that ACA resulted in significant microglia activation in the ventral horn of the lumbar spinal cord.…”

Metformin Promotes Axon Regeneration after Spinal Cord Injury through Inhibiting Oxidative Stress and Stabilizing Microtubule

“…SCI is a serious neurological disease that can induce neurological dysfunction and permanent damage. Series of secondary injuries, including oxidative stress, mitochondrial dysfunction, and neuronal cell apoptosis, are considered as the major factor for disability [47]. Thus, new effective therapeutic treatments for reducing SCI-induced neurological disorders and tissue damages are urgently needed.…”

Coenzyme Q10 Regulation of Apoptosis and Oxidative Stress in H2O2 Induced BMSC Death by Modulating the Nrf-2/NQO-1 Signaling Pathway and Its Application in a Model of Spinal Cord Injury

“…It not only affects the physical and mental health of patients but is also an economic burden on the family [1][2][3]. At present, although various pharmacological therapies are used for SCI, functional recovery is still uncertain [4][5][6].…”