Neuroreport · 2026
Laminarin attenuates cerebral ischemia-reperfusion injury by inhibiting Notch1 signaling and reprogramming microglial inflammatory responses.
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Chen Dingzhi, Xie Jieqiong, Wu Xiaohui, Kong Deyan, Luo Jiefeng
Аннотация
BACKGROUND: Neuroinflammation contributes to cerebral ischemia-reperfusion injury, and microglial inflammatory responses are regulated in part by Notch signaling. This study investigated whether laminarin, a brown algae-derived β-glucan polysaccharide, protects against cerebral ischemia-reperfusion injury by modulating Notch1-dependent microglial responses.
METHODS: A rat middle cerebral artery occlusion/reperfusion model was established, and laminarin was administered intraperitoneally at 10 mg/kg for seven consecutive days. Neurological deficits and infarct volume were assessed by modified neurological severity score and 2,3,5-triphenyltetrazolium chloride staining. Transcriptomic and bioinformatic analyses were used to identify laminarin-associated pathways. BV2 microglial cells were stimulated with lipopolysaccharide, and Jagged1 was used to reactivate Notch signaling. Inducible nitric oxide synthase (iNOS), Arginase 1 (Arg1), Notch pathway proteins, and inflammatory cytokines were examined by immunofluorescence, western blotting, and enzyme-linked immunosorbent assay.
RESULTS: Laminarin reduced infarct volume and improved neurological recovery in rats. Bioinformatic analysis and immunofluorescence indicated involvement of the Notch pathway. In vivo and in vitro, laminarin decreased iNOS-associated pro-inflammatory activation and increased Arg1-associated reparative responses, accompanied by reduced Notch1/Hes1/Hes5 activation. Jagged1 attenuated these effects and partially reversed laminarin-mediated changes in inflammatory markers and cytokine production.
CONCLUSION: Laminarin attenuates cerebral ischemia-reperfusion injury by reprogramming microglial inflammatory responses, at least partly through inhibition of the Notch1/Hes1/Hes5 signaling pathway. These findings support laminarin as a potential marine-derived immunomodulatory candidate for ischemic stroke research.
METHODS: A rat middle cerebral artery occlusion/reperfusion model was established, and laminarin was administered intraperitoneally at 10 mg/kg for seven consecutive days. Neurological deficits and infarct volume were assessed by modified neurological severity score and 2,3,5-triphenyltetrazolium chloride staining. Transcriptomic and bioinformatic analyses were used to identify laminarin-associated pathways. BV2 microglial cells were stimulated with lipopolysaccharide, and Jagged1 was used to reactivate Notch signaling. Inducible nitric oxide synthase (iNOS), Arginase 1 (Arg1), Notch pathway proteins, and inflammatory cytokines were examined by immunofluorescence, western blotting, and enzyme-linked immunosorbent assay.
RESULTS: Laminarin reduced infarct volume and improved neurological recovery in rats. Bioinformatic analysis and immunofluorescence indicated involvement of the Notch pathway. In vivo and in vitro, laminarin decreased iNOS-associated pro-inflammatory activation and increased Arg1-associated reparative responses, accompanied by reduced Notch1/Hes1/Hes5 activation. Jagged1 attenuated these effects and partially reversed laminarin-mediated changes in inflammatory markers and cytokine production.
CONCLUSION: Laminarin attenuates cerebral ischemia-reperfusion injury by reprogramming microglial inflammatory responses, at least partly through inhibition of the Notch1/Hes1/Hes5 signaling pathway. These findings support laminarin as a potential marine-derived immunomodulatory candidate for ischemic stroke research.