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  4. Insulin‑incubated palladium clusters promote recovery after brain injury

Insulin‑incubated palladium clusters promote recovery after brain injury

Journal of Nanobiotechnology, 2022 · DOI: https://doi.org/10.1186/s12951-022-01495-6 · Published: June 4, 2022

PharmacologyNeurologyBiomedical

Simple Explanation

Traumatic brain injury (TBI) can cause disability and death, and currently lacks specific treatments. The release of excess reactive oxygen species (ROS) after injury leads to further pathological changes. The study explores eliminating ROS as a potential therapy. The researchers synthesized insulin-incubated palladium (Pd@insulin) clusters, approximately 3.2 nm in diameter, using a green biomimetic chemistry approach. These clusters demonstrated marked multiple ROS-scavenging ability and were rapidly excreted with negligible adverse effects. In a TBI mouse model, intravenous injection of Pd@insulin clusters effectively suppressed excessive ROS production in the injured cortex. This significantly rescued motor function, cognition, and spatial memory, mainly due to their ROS-scavenging ability which inhibited neuroinflammation and reduced neuronal loss.

Study Duration
Not specified
Participants
C57BL/6J mice
Evidence Level
Not specified

Key Findings

  • 1
    Insulin-incubated palladium clusters (Pd@insulin) were successfully synthesized using a green biomimetic method and exhibited excellent multiple ROS-scavenging ability.
  • 2
    Pd@insulin clusters effectively reduced ROS levels in the brains of TBI mice, leading to improved motor function, learning, and spatial memory.
  • 3
    The therapeutic effects of Pd@insulin are attributed to its ROS-scavenging ability, which inhibits excessive neuroinflammation, reduces cell apoptosis, and prevents neuronal loss.

Research Summary

The study introduces a novel biomimetic synthesis method for ultrasmall Pd nanoclusters (Pd@insulin) using insulin as a template, demonstrating its effectiveness in scavenging ROS and improving outcomes in a TBI mouse model. Pd@insulin clusters exhibited excellent ROS-scavenging ability, promoted neurogenesis, inhibited neuronal loss, restrained neuroinflammation, and suppressed apoptosis in the injured cortex of TBI mice. Transcriptome profiling revealed that Pd@insulin's therapeutic effect on TBI occurs via neuroinflammation inhibition, particularly by modulating the inflammatory responses of microglia.

Practical Implications

Clinical Translation Potential

The simple structure, easy synthesis, low toxicity, and rapid metabolism of Pd@insulin clusters may facilitate their clinical translation for TBI treatment.

Treatment of ROS-Related Diseases

The biomimetic and scalable process used to synthesize Pd@insulin could inspire the development of other nanodrugs for treating TBI or other ROS-related diseases.

Targeted Nanodrug Delivery

Using insulin to facilitate BBB penetration of nanoparticles may lead to more effective targeted nanodrug delivery strategies for brain injuries and disorders.

Study Limitations

  • 1
    The study primarily focuses on a mouse model, and further research is needed to determine the efficacy and safety of Pd@insulin clusters in humans.
  • 2
    The long-term effects and potential side effects of Pd@insulin treatment were not extensively investigated.
  • 3
    The specific mechanisms by which Pd@insulin interacts with and modulates microglia require further elucidation.

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