This study was designed to determine the effective therapeutic parameters and evaluate the regenerative potential of low-level laser therapy (LLLT) after traumatic spinal cord injuries (TSCIs) in animal studies. The EMBASE and MEDLINE databases were searched on October 5, 2019, and followed with an update on January 2, 2021. All animal studies discussing the effect of LLLT on main pathophysiological events after TSCI, including inflammation, axon growth, remyelination, glial scar formation, cavity size, and locomotor recovery, were included. For statistical analysis, we used mean difference with 95% confidence intervals for locomotor recovery. In total, 19 articles were included based on our criteria. The results showed that regardless of laser type, laser beams with a wavelength between 600 and 850 nm significantly suppress inflammation and led inflammatory cells to M2 polarization and wound healing. Also, laser therapy using these wavelengths for more than 2 weeks significantly improved axon regeneration and remyelination. Improvement of locomotor recovery was more efficient using wavelengths less than 700 nm (SMD = 1.21; 95%CI: 0.09, 2.33; p = 0.03), lasers with energy densities less than 100 J/cm (SMD = 1.72; 95%CI: 0.84, 2.59; p = 0.0001) and treatment duration between 1 and 2 weeks (SMD = 2.21; 95%CI: 1.24, 3.19; p < 0.00001). The LLLT showed promising potential to modulate pathophysiological events and recovery after TSCI, although there was heterogeneity in study design and reporting methods, which should be considered in future studies.
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http://dx.doi.org/10.1007/s10103-021-03301-5 | DOI Listing |
J Neuroinflammation
March 2025
Department of Orthopaedics, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, China.
Background: Recent studies have confirmed the critical role of neonatal microglia in wound healing and axonal regeneration following spinal cord injury (SCI). However, the limited migration of microglia to the center of adult lesion may significantly impede their potential benefits.
Methods: We established a model of microglial centripetal migration and prolonged retention in C57BL/6J and transgenic mice by injecting exogenous C-X3-C motif chemokine ligand 1 (CX3CL1) and macrophage colony-stimulating factor (M-CSF) directly into the lesion site post-SCI.
J Neuroinflammation
March 2025
Neuroscience Program, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
Spinal cord injury (SCI) can cause permanent dysfunction proceeding from multifaceted neuroinflammatory processes that contribute to damage and repair. Fidgetin-like 2 (FL2), a microtubule-severing enzyme that negatively regulates axon growth, microglial functions, and wound healing, has emerged as a potential therapeutic target for central nervous system injuries and neuroinflammation. To test the hypothesis that FL2 knockdown increases acute neuroinflammation and improves recovery after SCI, we examined the effects of nanoparticle-encapsulated FL2 siRNA treatment after a moderate contusion SCI in rats.
View Article and Find Full Text PDFMol Neurobiol
March 2025
Department of Orthopaedics, The First Affiliated Hospital of Kunming Medical University, Kunmingaq , Yunnan, 650032, China.
The outgrowth of motor neurons needs to be enhanced for the efficient recovery of sensory and movement abilities after nerve injury. The microRNA miR-124-3p can repair spinal cord injury (SCI) and promote neurite outgrowth. In this study, we aimed to investigate the effect of miR-124-3p on neurite outgrowth and the mechanism underlying its effect on SCI.
View Article and Find Full Text PDFJ Pharmacol Exp Ther
February 2025
Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, Arizona; Southern Arizona VA Health Care System, Tucson, Arizona; Department of Neuroscience, College of Medicine, University of Arizona, Tucson, Arizona; Southwest Environmental Health Science Center, University of Arizona, Tucson, Arizona; Center for Innovation in Brain Science, University of Arizona, Tucson, Arizona. Electronic address:
Secondary spinal cord injury (SCI) is characterized by increased cytokines and chemokines at the site of injury that have been associated with the development of neuropathic pain. Nearly 80% of SCI patients report suffering from chronic pain, which is poorly managed with available analgesics. While treatment with the US Food and Drug Administration-approved β-adrenergic receptor agonist formoterol improves various aspects of recovery post-SCI in vivo, its effects on cytokines, chemokines, and neuropathic pain remain unknown.
View Article and Find Full Text PDFJ Pharmacol Exp Ther
February 2025
Department of Pharmacology, School of Pharmacy, Qingdao University Medical College, Qingdao, China; Institute of Innovative Drugs, Qingdao University, Qingdao, China. Electronic address:
Genetic loss-of-function mutations of the Na1.7 channel, abundantly expressed in peripheral nociceptive neurons, cause congenital insensitivity to pain in humans, indicating that selective inhibition of the channel may lead to potential therapy for pain disorders. In this study, we investigated a novel compound, 5-chloro-N-(cyclopropylsulfonyl)-2-fluoro-4-(2-(8-(furan-2-ylmethyl)-8-azaspiro [4.
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