Stroke and vascular neurology · 2026
Lycium barbarum glycopeptide attenuates ischaemic stroke by inhibiting inflammation via SIRT3-mediated NLRP3 deacetylation.
СтатьяНазвание и аннотация: Перевод в очереди
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Han Bo, Ma Changsheng, Zhang Liying, Meng Shuchen, Bai Min, Yu Zhexiong, Duan Mengyuan, Liu Jiaqi, Guo Jinfen, Shi Changku, He Maotao, Liu Yongping
Аннотация
BACKGROUND: Inflammatory processes play a critical role in ischaemic stroke. Acetylation of NLRP3 is a key step in amplifying neuroinflammation.(LbGP), a bioactive glycoprotein derived from Lycium barbarum, has anti-inflammatory potential, but its mechanisms in post-stroke neuroinflammation remain unclear.
AIM: This study aimed to investigate the efficacy and molecular mechanisms of LbGP in alleviating neuroinflammation following ischaemic stroke.
METHODS: A mouse model of middle cerebral artery occlusion (MCAO)/reperfusion was used to induce focal cerebral ischaemia/reperfusion (I/R) injury. Microglial cells were subjected to oxygen-glucose deprivation/reoxygenation. Neurological recovery was assessed by Y-maze and open-field tests. Molecular mechanisms were explored using Western blotting, ELISA, co-immunoprecipitation and immunofluorescence.
RESULTS: LbGP significantly reduced cerebral infarct volume, attenuated neuroinflammation and improved functional recovery in I/R mice. Mechanistically, LbGP suppressed NLRP3 inflammasome activation through Sirtuin 3-mediated inhibition of NLRP3 acetylation, a finding further validated by exacerbated neuroinflammation in Sirt3-knockout mice.
CONCLUSION: This study demonstrates for the first time that LbGP alleviates post-stroke neuroinflammation via Sirt3-mediated deacetylation of NLRP3, thereby disrupting inflammasome activation, and identifies LbGP as a promising therapeutic candidate for ischaemic stroke.
AIM: This study aimed to investigate the efficacy and molecular mechanisms of LbGP in alleviating neuroinflammation following ischaemic stroke.
METHODS: A mouse model of middle cerebral artery occlusion (MCAO)/reperfusion was used to induce focal cerebral ischaemia/reperfusion (I/R) injury. Microglial cells were subjected to oxygen-glucose deprivation/reoxygenation. Neurological recovery was assessed by Y-maze and open-field tests. Molecular mechanisms were explored using Western blotting, ELISA, co-immunoprecipitation and immunofluorescence.
RESULTS: LbGP significantly reduced cerebral infarct volume, attenuated neuroinflammation and improved functional recovery in I/R mice. Mechanistically, LbGP suppressed NLRP3 inflammasome activation through Sirtuin 3-mediated inhibition of NLRP3 acetylation, a finding further validated by exacerbated neuroinflammation in Sirt3-knockout mice.
CONCLUSION: This study demonstrates for the first time that LbGP alleviates post-stroke neuroinflammation via Sirt3-mediated deacetylation of NLRP3, thereby disrupting inflammasome activation, and identifies LbGP as a promising therapeutic candidate for ischaemic stroke.