N-acetylcysteine treatment following spinal cord trauma reduces neural tissue damage and improves locomotor function in mice

Abstract

Following spinal cord trauma, mitochondrial dysfunction associated with increased oxidative stress is a critical event leading to leukocyte inflammatory responses, neuronal cell death and demyelination, contributing to permanent locomotor and neurological disability. The present study demonstrated that the mitochondrial enhancer N-acetylcysteine (NAC) may restore redox balance via enhancement of mitochondrial respiratory activity following traumatic spinal cord injury (SCI). In addition, NAC ameliorates oxidative stress-induced neuronal loss, demyelination, leukocyte infiltration and inflammatory mediator expression and improves long-term locomotor function. Furthermore, neuronal survival and neurological recovery are significantly correlated with increased mitochondrial bioenergetics in SCI following treatment with NAC. Therefore, NAC may represent a potential therapeutic agent for preserving mitochondrial dynamics and integrity following traumatic SCI.

Bone Morphogenic Protein-2 (rhBMP2)-Loaded Silk Fibroin Scaffolds to Enhance the Osteoinductivity in Bone Tissue Engineering

“…Ample mechanical strength is a property essential for a tissue scaffold. Blending of pure SF increased the flexibility of nanofiber in our experiment, and previous reports also revealed a similar trend in improvement of mechanical properties upon blending of SF with other materials to yield employable blended biomaterials [ 21 , 23 ]. So, our fabricated scaffold possesses essential mechanical strength and flexibility which is required in tissue engineering applications.…”

Low-level laser facilitates alternatively activated macrophage/microglia polarization and promotes functional recovery after crush spinal cord injury in rats

“…Neuronal cell loss is a disastrous secondary damage following SCI, which leads to neurological deficits 45 , 46 . The amelioration of this phenomenon allows for some rehabilitation in SCI animal models 47 – 49 . In the present study, interestingly, the number of surviving neurons significantly increased in the LLLT group in the rostral and caudal side, suggesting that LLLT has a general protective effect on neurons after injury.…”

Adjunctive N-acetylcysteine in depression: exploration of interleukin-6, C-reactive protein and brain-derived neurotrophic factor

“…NAC is also a potent antioxidant and the therapeutic capacity of NAC to restore mitochondrial dysfunction has been well documented in preclinical studies (31–34). Mitochondrial dysfunction could mediate increases in production of reactive oxidative and nitrosative species, and subsequently contribute to increases in production of pro-inflammatory cytokines, DNA damage and lipid peroxidation (11,33,35).…”