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<p>Spontaneous subarachnoid hemorrhage (SAH) remains a life-threatening type of hemorrhagic stroke. Astrocytes are key cellular responders after SAH. We designed the current study to elucidate the global astrocyte reaction with an emphasis on the proinflammatory reaction following SAH. We used an animal model of SAH by applying non-heparinized autologous blood to the cisterna magna. Elevated intracranial pressure after SAH was mimicked by using artificial cerebrospinal fluid (ACSF) instead of blood. We mapped the length and the number of astrocytic processes using immunohistochemical staining of glial fibrillary acidic proteins (GFAP) to detect astrocytes. To monitor proinflammatory changes in the astrocytes we used double immunohistochemical of GFAP along with NF-κB, TNF-α, IL-1β, IL-6 and STAT3. Immunohistochemical methods showed increased GFAP levels, and astrocytic processes were longer and more numerous mainly 7 and 14 days after SAH induction or ACSF application. The levels of NF-κB, TNF-α, IL-1β, IL-6 and STAT3 in astrocytes were globally increased at different time periods not only following SAH induction but also after ACSF application. Our results highlight a critical role for astrocytes in mediating widespread gliosis and neuroinflammation following SAH. Modulation of astrocyte function may therefore be a potential therapeutic target for reducing secondary brain damage following SAH.</p>

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Astrocyte activation and gliosis contribute to brain-wide neuroinflammation following experimental subarachnoid hemorrhage

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月27日

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  • Peter Solár,
  • Martin Bareš,
  • Alemeh Zamani,
  • Lucie Kubíčková,
  • Klaudia Hašanová,
  • Ivana Pračková,
  • Anna Rábová,
  • Marek Joukal

摘要

Spontaneous subarachnoid hemorrhage (SAH) remains a life-threatening type of hemorrhagic stroke. Astrocytes are key cellular responders after SAH. We designed the current study to elucidate the global astrocyte reaction with an emphasis on the proinflammatory reaction following SAH. We used an animal model of SAH by applying non-heparinized autologous blood to the cisterna magna. Elevated intracranial pressure after SAH was mimicked by using artificial cerebrospinal fluid (ACSF) instead of blood. We mapped the length and the number of astrocytic processes using immunohistochemical staining of glial fibrillary acidic proteins (GFAP) to detect astrocytes. To monitor proinflammatory changes in the astrocytes we used double immunohistochemical of GFAP along with NF-κB, TNF-α, IL-1β, IL-6 and STAT3. Immunohistochemical methods showed increased GFAP levels, and astrocytic processes were longer and more numerous mainly 7 and 14 days after SAH induction or ACSF application. The levels of NF-κB, TNF-α, IL-1β, IL-6 and STAT3 in astrocytes were globally increased at different time periods not only following SAH induction but also after ACSF application. Our results highlight a critical role for astrocytes in mediating widespread gliosis and neuroinflammation following SAH. Modulation of astrocyte function may therefore be a potential therapeutic target for reducing secondary brain damage following SAH.