Selenium nanoparticles derived from Proteus mirabilis YC801 alleviate oxidative stress and inflammatory response to promote nerve repair in rats with spinal cord injury.
Xiangyu LiuYingji MaoShengwei HuangWeifeng LiWei ZhangJingzhou AnYongchao JinJianzhong GuanLifang WuPinghui ZhouPublished in: Regenerative biomaterials (2022)
Microbial biotransformation and detoxification of biotoxic selenite into selenium nanoparticles (SeNPs) has emerged as an efficient technique for the utilization of selenium. SeNPs are characterized by high bioavailability and have several therapeutic effects owing to their antioxidant, anti-inflammatory and neuroprotective activities. However, their influence on microenvironment disturbances and neuroprotection after spinal cord injury (SCI) is yet to be elucidated. This study aimed to assess the influence of SeNPs on SCI and explore the underlying protective mechanisms. Overall, the proliferation and differentiation of neural stem cells were facilitated by SeNPs derived from Proteus mirabilis YC801 via the Wnt/β-catenin signaling pathway. The SeNPs increased the number of neurons to a greater extent than astrocytes after differentiation and improved nerve regeneration. A therapeutic dose of SeNPs remarkably protected the integrity of the spinal cord to improve the motor function of the hind limbs after SCI and decreased the expression of several inflammatory factors such as tumor necrosis factor-α and interleukin-6 in vivo and enhanced the production of M2-type macrophages by regulating their polarization, indicating the suppressed inflammatory response. Besides, SeNPs reversed the SCI-mediated production of reactive oxygen species. In conclusion, SeNPs treatment holds the potential to improve the disturbed microenvironment and promote nerve regeneration, representing a promising therapeutic approach for SCI.
Keyphrases
- spinal cord injury
- oxidative stress
- stem cells
- spinal cord
- inflammatory response
- anti inflammatory
- reactive oxygen species
- neural stem cells
- rheumatoid arthritis
- peripheral nerve
- neuropathic pain
- dna damage
- signaling pathway
- ischemia reperfusion injury
- risk assessment
- cell proliferation
- diabetic rats
- cerebral ischemia
- blood brain barrier
- binding protein
- lps induced