Pathology, research and practice · 2025
Fucoxanthin alleviates secondary brain injury in mice following intracerebral hemorrhage via PI3K-mediated inhibition of NF-κB signaling pathway.
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Liu WeiBing, Xu WenHua
Аннотация
BACKGROUND: ICH is an acute clinical cerebrovascular disease without effective treatments. This study was designed to investigate the therapeutic value of fucoxanthin in ICH treatment.
METHODS: Animal ICH models were established by collagenase IV injection. ICH mice were given intraperitoneal injection of fucoxanthin (100 mg/kg). Neurological deficits, brain edema, blood-brain barrier (BBB) integrity, and histological impairment were assessed. Nissl staining and TUNEL staining were performed to detect neuronal cell loss and apoptosis. The levels of tight junction proteins, apoptosis-related proteins, Iba-1, and pathway-related proteins were measured by immunofluorescence staining, western blotting, and ELISA.
RESULTS: Fucoxanthin administration attenuated neurological deficits and brain injuries following ICH. Additionally, fucoxanthin alleviated neuronal apoptosis caused by ICH. Moreover, fucoxanthin inhibited microglia-mediated inflammation and M1 polarization in ICH models. Mechanistically, fucoxanthin inactivated the NF-κB pathway and triggered the activation of PI3K/Akt signaling after ICH, and LY294002 (a PI3K inhibitor) compromised the protective effect of fucoxanthin.
CONCLUSION: Fucoxanthin alleviates ICH-induced neurological deficits and brain injuries by suppressing the PI3K/Akt-mediated NF-κB pathway to inhibit M1 polarization and attenuate neuroinflammation, neuronal apoptosis, BBB dysfunction, and brain edema.
METHODS: Animal ICH models were established by collagenase IV injection. ICH mice were given intraperitoneal injection of fucoxanthin (100 mg/kg). Neurological deficits, brain edema, blood-brain barrier (BBB) integrity, and histological impairment were assessed. Nissl staining and TUNEL staining were performed to detect neuronal cell loss and apoptosis. The levels of tight junction proteins, apoptosis-related proteins, Iba-1, and pathway-related proteins were measured by immunofluorescence staining, western blotting, and ELISA.
RESULTS: Fucoxanthin administration attenuated neurological deficits and brain injuries following ICH. Additionally, fucoxanthin alleviated neuronal apoptosis caused by ICH. Moreover, fucoxanthin inhibited microglia-mediated inflammation and M1 polarization in ICH models. Mechanistically, fucoxanthin inactivated the NF-κB pathway and triggered the activation of PI3K/Akt signaling after ICH, and LY294002 (a PI3K inhibitor) compromised the protective effect of fucoxanthin.
CONCLUSION: Fucoxanthin alleviates ICH-induced neurological deficits and brain injuries by suppressing the PI3K/Akt-mediated NF-κB pathway to inhibit M1 polarization and attenuate neuroinflammation, neuronal apoptosis, BBB dysfunction, and brain edema.