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Related Concept Videos

Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

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Low-Intensity Pulsed Ultrasound Promotes Spinal Cord Injury Recovery by Regulating Microglia-Mediated

Xiaoyu Li1, Yang Liu1, Wanghui Liu1

  • 1Department of Orthopedics, Shanghai Changhai Hospital, Shanghai, China.

CNS Neuroscience & Therapeutics
|March 28, 2026
PubMed
Summary

Low-intensity pulsed ultrasound (LIPUS) effectively reduces neuroinflammation and promotes motor function recovery after spinal cord injury (SCI) in rats. This noninvasive therapy modulates microglia-mediated inflammation via specific signaling pathways and gene expression, offering a promising treatment for SCI.

Keywords:
bioinformatics analysisinflammationlow‐intensity pulsed ultrasoundmicrogliaspinal cord injury

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Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Biophysics

Background:

  • Spinal cord injury (SCI) involves complex primary and secondary injury phases, with neuroinflammation critically driving secondary damage through microglia and peripheral immune cell interactions.
  • Low-intensity pulsed ultrasound (LIPUS) is a noninvasive physical therapy with demonstrated potential in inflammation regulation and angiogenesis, suggesting its utility for SCI intervention.
  • The precise therapeutic effects and molecular mechanisms of LIPUS in SCI treatment remain underexplored.

Purpose of the Study:

  • To investigate the therapeutic efficacy of LIPUS in a rat model of spinal cord injury.
  • To elucidate the underlying molecular mechanisms by which LIPUS modulates neuroinflammation and promotes functional recovery after SCI.
  • To identify potential therapeutic targets and signaling pathways involved in LIPUS treatment for SCI.

Main Methods:

  • Establishment of a T10 spinal cord injury (SCI) model in 88 Sprague-Dawley rats, randomly assigned to sham, SCI, or SCI + LIPUS groups.
  • Evaluation of hindlimb motor function using Basso, Beattie, and Bresnahan (BBB) scores, alongside histological and immunofluorescence analyses of spinal cord tissues.
  • In vitro studies using lipopolysaccharide-induced BV2 microglial models and Transwell co-cultures with HT22 neurons to assess cell viability, inflammatory markers, and neuronal apoptosis, complemented by RNA sequencing and bioinformatics analysis.

Main Results:

  • LIPUS treatment, particularly with parameters of 180 mW/cm² and 1.5 MHz, significantly improved hindlimb motor function in SCI rats from day 7 to day 28 post-injury.
  • Histological analysis revealed LIPUS reduced spinal cord cavity area, inhibited microglial activation, promoted M2 polarization, and alleviated secondary inflammation.
  • In vitro findings confirmed LIPUS enhanced microglial viability, upregulated anti-inflammatory factors (IL-10, Arg-1), downregulated pro-inflammatory factors (IL-6, TNF-α), and reduced neuronal apoptosis. RNA sequencing identified key pathways (NOD-like receptor, IL-17) and hub genes (e.g., CXCR2) modulated by LIPUS.

Conclusions:

  • LIPUS effectively alleviates neuroinflammation and promotes neurological recovery following SCI by regulating microglia-mediated inflammatory responses.
  • The therapeutic mechanism involves modulation of the NOD-like receptor and IL-17 signaling pathways, along with the downregulation of specific hub genes like CXCR2.
  • This study provides a scientific rationale for the clinical application of LIPUS in SCI treatment and supports the development of combined therapeutic strategies.