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<p>Sinomenine (SIN) has been established to exert neuroprotective effects in ischemic stroke (IS), yet its specific molecular targets and detailed mechanisms remain incompletely understood. This study identified Fermt2 as a critical target through which SIN exerted its neuroprotective effects in IS. In a rat model of cerebral ischemia-reperfusion injury, overexpression of Fermt2 improved neurological deficits, reduced cerebral infarct volume by nearly one-third, and significantly decreased neuronal apoptosis in the ischemic penumbra. In vitro and in vivo experiments demonstrated that upregulation of Fermt2 promoted a shift in microglial polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, thereby suppressing pro-inflammatory cytokines and restoring anti-inflammatory factors. Mechanistic investigations revealed that Fermt2 functioned by inhibiting the RhoA/ROCK/NF-κB signaling pathway. Crucially, knockdown of Fermt2 reversed the beneficial effects of SIN in IS rats. In conclusion, Fermt2 is a master regulator of microglia-dependent neuroinflammation and a promising therapeutic target for IS.</p>

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Neuroprotective Mechanisms of Sinomenine in Ischemic Stroke: The Role of Fermt2 in Neuroinflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月5日

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  • Jie Yan,
  • Wenjuan Li,
  • Tian Qin,
  • Haimin Ye,
  • Congling Chen,
  • Ling Li,
  • Yehui Liu

摘要

Sinomenine (SIN) has been established to exert neuroprotective effects in ischemic stroke (IS), yet its specific molecular targets and detailed mechanisms remain incompletely understood. This study identified Fermt2 as a critical target through which SIN exerted its neuroprotective effects in IS. In a rat model of cerebral ischemia-reperfusion injury, overexpression of Fermt2 improved neurological deficits, reduced cerebral infarct volume by nearly one-third, and significantly decreased neuronal apoptosis in the ischemic penumbra. In vitro and in vivo experiments demonstrated that upregulation of Fermt2 promoted a shift in microglial polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, thereby suppressing pro-inflammatory cytokines and restoring anti-inflammatory factors. Mechanistic investigations revealed that Fermt2 functioned by inhibiting the RhoA/ROCK/NF-κB signaling pathway. Crucially, knockdown of Fermt2 reversed the beneficial effects of SIN in IS rats. In conclusion, Fermt2 is a master regulator of microglia-dependent neuroinflammation and a promising therapeutic target for IS.