Polysaccharide from Laminaria japonica Alleviates Acute Neuroinflammation in Cerebral Ischemia-Reperfusion Injury via Csf3-Related Mechanisms - Report - MDSpire

Polysaccharide from Laminaria japonica Alleviates Acute Neuroinflammation in Cerebral Ischemia-Reperfusion Injury via Csf3-Related Mechanisms

  • By

  • Tangming Guan

  • Siyu Chen

  • Dongbo Jiang

  • Weiming Cai

  • Huayan Chen

  • Yan Wang

  • Kefeng Wu

  • Xin Zhou

  • April 23, 2026

  • 0 min

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Clinical Report: Polysaccharide from Laminaria japonica Alleviates Acute Neuroinflammation

Overview

Laminaria japonica polysaccharide (LJP) demonstrates neuroprotective effects in a mouse model of cerebral ischemia/reperfusion injury by reducing infarct volume and improving neurological function. The mechanism involves modulation of granulocyte colony-stimulating factor (Csf3), indicating its potential as a therapeutic agent for ischemic stroke.

Background

Cerebral ischemia/reperfusion injury is a significant cause of secondary brain damage, primarily driven by neuroinflammation and microglial activation. Current therapies focus on restoring blood flow but do not effectively address the inflammatory processes that exacerbate neuronal injury. The exploration of marine-derived polysaccharides like LJP offers a novel approach to mitigate these inflammatory responses.

Data Highlights

ParameterEffect of LJP
Infarct VolumeReduced
Neurological FunctionImproved
Microglial Pro-inflammatory PolarizationSuppressed
IL-1b LevelsDecreased
TNFα LevelsDecreased
IL-6 LevelsDecreased

Key Findings

  • LJP is structurally characterized by high fucose, galacturonic acid, glucuronic acid, and sulfate content.
  • Administration of LJP significantly reduced infarct volume in a mouse model of tMCAO.
  • LJP improved neurological function and suppressed microglial pro-inflammatory polarization.
  • Levels of pro-inflammatory cytokines IL-1b, TNFα, and IL-6 were decreased following LJP treatment.
  • Csf3 was identified as a potential mediator of LJP's effects, with recombinant Csf3 partially reversing its protective benefits.
  • Csf3-specific antibodies did not enhance LJP's anti-inflammatory effects, indicating a complex role for Csf3 in this context.

Clinical Implications

The findings suggest that LJP may serve as a complementary therapeutic agent in the management of ischemic stroke by targeting neuroinflammation. Further investigation into its mechanisms and potential clinical applications could enhance treatment strategies for stroke patients.

Conclusion

Reiterate the importance of further research on LJP's mechanisms and potential clinical applications.

References

  1. Fang et al., Marine Drugs, 2020 -- Modulation of Macrophage Polarization by LJP
  2. 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association
  3. Granulocyte-Colony Stimulating Factor (G-CSF) for stroke: an individual patient data meta-analysis - PMC
  4. Basic Research in Cardiology — Inhibition of Acid Sphingomyelinase Following Ischemia Enhances Brain Angiogenesis and Remodeling via Small Extracellular Vesicles
  5. Basic Research in Cardiology — Deficiency of Homozygous Smpd1 Exacerbates Brain Ischemia/Reperfusion Injury Through Polymorphonuclear Neutrophil Mechanisms, While Heterozygous Smpd1 Deficiency Offers Protection Against Mild Focal Cerebral Ischemia
  6. Acta Neuropathologica — Overexpression of Heparanase Disrupts Inflammatory Responses and Macrophage Clearance of Amyloid-β in Mouse Brain
  7. Acta Neuropathologica — Inflammation Following Stroke: A Potential Therapeutic Target or a Beneficial Mechanism?
  8. 2026 AHA/ASA Early Management of Ischemic Stroke
  9. Granulocyte-Colony Stimulating Factor (G-CSF) for stroke: an individual patient data meta-analysis - PMC

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