Neuroprotective Mechanisms of Sinomenine in Ischemic Stroke: The Role of Fermt2 in Neuroinflammation.
- 1Department of Neurology, The Second Affiliated Hospital of Hunan, University of Chinese Medicine, Changsha, Hunan, 410005, China.
- 2Department of Neurology, The Second Affiliated Hospital of Hunan, University of Chinese Medicine, Changsha, Hunan, 410005, China. [email protected].
Abstract
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.
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BibTeX
@article{yan2026neuroprotective,
title = {{Neuroprotective Mechanisms of Sinomenine in Ischemic Stroke: The Role of Fermt2 in Neuroinflammation.}},
author = {Jie Yan and Wenjuan Li and Tian Qin and Haimin Ye and Congling Chen and Ling Li and Yehui Liu},
journal = {Inflammation},
year = {2026},
month = aug,
doi = {10.1007/s10753-026-02556-w},
url = {https://europepmc.org/article/MED/42967958},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Neuroprotective Mechanisms of Sinomenine in Ischemic Stroke: The Role of Fermt2 in Neuroinflammation.
AU - Jie Yan
AU - Wenjuan Li
AU - Tian Qin
AU - Haimin Ye
AU - Congling Chen
AU - Ling Li
AU - Yehui Liu
PY - 2026
DA - 2026/08/05
JO - Inflammation
DO - 10.1007/s10753-026-02556-w
UR - https://europepmc.org/article/MED/42967958
AB - 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.
SN - 0360-3997
SN - 1573-2576
ER -