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<p>Intracerebral hemorrhage (ICH) is a devastating stroke subtype leading to severe sensorimotor dysfunction. Many studies showed that microglia phagocytosis could promote hematoma absorption, and scavenger receptors expressed on microglia were associated with its phagocytosis. As a specific phagocytic receptor, blocking the P2Y6 receptor (P2Y6R) with MRS2578 (3&#xa0;mg/kg) could inhibit the phagocytic activity of microglia, which had been reported in a variety of neurological disorders, such as cerebral ischemia, Parkinson’s diseases and neurodegenerative diseases. But the effects of P2Y6R-mediated microglia phagocytosis on the prognosis of ICH are still lacking. In the present study, we showed that P2Y6R expression elevated and peaked at day 3 after ICH. And treatment with MRS2578 (3&#xa0;mg/kg) for three consecutive days could impair the phagocytosis of microglia, accompanied by delayed hematoma absorption rate, aggravated brain edema and blood–brain barrier disruption, as well as impaired neurological deficit in ICH mice. MRS2578 treatment also increased the expression of pro-inflammatory factors (TNF-α, iNOS) after ICH. Furthermore, MRS2578 treatment further increased the expression of NF-<i>κ</i>B, which regulates the expression of these pro-inflammatory cytokines. In summary, our results suggested that regulating microglial phagocytosis could improve the prognosis of ICH, and P2Y6R offered a meaningful target.</p>

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Inhibition of P2Y6 Receptor-Mediated Microglia Phagocytosis Aggravates Brain Injury in Mice of Intracerebral Hemorrhage

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月8日

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  • Ying Xu,
  • Weiya Li,
  • Jing Zhang,
  • Weiwei Gao,
  • Ting Zhang,
  • Qing Chen,
  • Nan Wang,
  • Yongjia Zhou,
  • Fengjiao Zhang,
  • Jiahao Qin

摘要

Intracerebral hemorrhage (ICH) is a devastating stroke subtype leading to severe sensorimotor dysfunction. Many studies showed that microglia phagocytosis could promote hematoma absorption, and scavenger receptors expressed on microglia were associated with its phagocytosis. As a specific phagocytic receptor, blocking the P2Y6 receptor (P2Y6R) with MRS2578 (3 mg/kg) could inhibit the phagocytic activity of microglia, which had been reported in a variety of neurological disorders, such as cerebral ischemia, Parkinson’s diseases and neurodegenerative diseases. But the effects of P2Y6R-mediated microglia phagocytosis on the prognosis of ICH are still lacking. In the present study, we showed that P2Y6R expression elevated and peaked at day 3 after ICH. And treatment with MRS2578 (3 mg/kg) for three consecutive days could impair the phagocytosis of microglia, accompanied by delayed hematoma absorption rate, aggravated brain edema and blood–brain barrier disruption, as well as impaired neurological deficit in ICH mice. MRS2578 treatment also increased the expression of pro-inflammatory factors (TNF-α, iNOS) after ICH. Furthermore, MRS2578 treatment further increased the expression of NF-κB, which regulates the expression of these pro-inflammatory cytokines. In summary, our results suggested that regulating microglial phagocytosis could improve the prognosis of ICH, and P2Y6R offered a meaningful target.