CNS neuroscience & therapeutics · 2025
H2S Donor SPRC Ameliorates Ischemic Stroke by Upregulating CD24.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wang Chenye, Li Sha, Li Qixiu, Xi Haiyan, Li Jiejia, Zhu Qing, Wu Pinwen, Zhu Yi-Zhun, Mao Yicheng
Аннотация
BACKGROUND: Ischemic stroke is well-known for its high mortality and morbidity, but its treatment remains to be explored due to the current limitations. For example, severe neuroinflammation occurs after ischemic stroke; however, effective neuroinflammatory inhibitors are still lacking. Thus, the development of new therapeutic targets of inhibiting neuroinflammation is urgent. CD24 is a small heavy glycosylated protein, which plays a critical role in neural development and acts as an inflammatory suppressor in tumors and autoimmune diseases. But the role of CD24 in ischemic stroke remains unknown.
AIMS: The role of CD24 in ischemic stroke should be explored. Additionally, the potential relationship between the H2S donor, S-propargyl-cysteine (SPRC) and CD24 in ischemic stroke should be revealed.
METHODS: Mechanism studies have been performed both in vitro and in vivo to verify the CD24-mediated inflammation and migration. SPRC has been applied to treat ischemic stroke, and its potential association with CD24 has been studied.
RESULTS: The overexpression of CD24 can inhibit the nuclear factor kappa B (NF-κB) inflammatory signaling pathway and promote the migration ability of M2 microglia cells via Src/Fak/Pyk2 signaling pathway in an inflammatory model of BV2 cells. SPRC can upregulate the level of endogenous H2S via cystathionase-β-synthase (CBS) and it indirectly plays a role in upregulating CD24.
CONCLUSIONS: CD24 could be a potential target of inhibiting neuroinflammation. SPRC reduces inflammation in ischemic stroke by regulating the CD24/Iκ-Bα/NF-κB inflammatory signaling pathway and improves the migration ability of M2 microglia via CD24/Src/Fak/Pyk2 signaling pathway, which further alleviates the inflammatory response at the lesion.
AIMS: The role of CD24 in ischemic stroke should be explored. Additionally, the potential relationship between the H2S donor, S-propargyl-cysteine (SPRC) and CD24 in ischemic stroke should be revealed.
METHODS: Mechanism studies have been performed both in vitro and in vivo to verify the CD24-mediated inflammation and migration. SPRC has been applied to treat ischemic stroke, and its potential association with CD24 has been studied.
RESULTS: The overexpression of CD24 can inhibit the nuclear factor kappa B (NF-κB) inflammatory signaling pathway and promote the migration ability of M2 microglia cells via Src/Fak/Pyk2 signaling pathway in an inflammatory model of BV2 cells. SPRC can upregulate the level of endogenous H2S via cystathionase-β-synthase (CBS) and it indirectly plays a role in upregulating CD24.
CONCLUSIONS: CD24 could be a potential target of inhibiting neuroinflammation. SPRC reduces inflammation in ischemic stroke by regulating the CD24/Iκ-Bα/NF-κB inflammatory signaling pathway and improves the migration ability of M2 microglia via CD24/Src/Fak/Pyk2 signaling pathway, which further alleviates the inflammatory response at the lesion.