Stroke and Vascular Neurology · Published 2026-08-03 · DOI 10.1136/svn-2026-005321
Bo Han, Changsheng Ma, Liying Zhang, Shuchen Meng, Min Bai, Zhexiong Yu, Mengyuan Duan, Jiaqi Liu, Jinfen Guo, Changku Shi, Maotao He, Yongping Liu
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.
Abstract from DOAJ. Public domain (CC0 1.0).
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Han, B., Ma, C., Zhang, L., et al. (2026). Lycium barbarum glycopeptide attenuates ischaemic stroke by inhibiting inflammation via SIRT3-mediated NLRP3 deacetylation. Stroke and Vascular Neurology. https://doi.org/10.1136/svn-2026-005321