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EGCG-loaded nanoparticles attenuate post-SAH white matter injury by targeting HO-1/S100A10 to suppress oxidative
Dongcen Lang1, Yanning Zheng1, Jing Zhang1
1College of Life Sciences, Henan Normal University, Xinxiang, Henan, People's Republic of China.
Objective:
Subarachnoid hemorrhage (SAH) is associated with high mortality and poor outcomes, which are closely related to white matter injury (WMI). (-)-Epigallocatechin-3-gallate (EGCG) exerts neuroprotective effects by inhibiting oxidative stress-related ferroptosis in astrocytes and improving neurological function. However, the role and mechanism of EGCG in regulating reactive astrocytes (RAs) to alleviate WMI after SAH remain unclear.
Methods:
A mouse model of SAH was used to evaluate the effects of EGCG-loaded nanoparticles (EGCG-NPs). Western blot, qPCR, and immunofluorescence were performed for biochemical analysis. Neurological function was assessed using neurological deficit scores and the Morris water maze test.
Results:
Following SAH, HO-1-mediated iron accumulation and ROS production promoted A1/A2 reactive astrocyte polarization, resulting in myelination damage and aggravated WMI. Knockdown of S100A10 inhibited iron-dependent oxidative stress in RAs and attenuated WMI. EGCG-NPs significantly suppressed HO-1/S100A10-mediated iron overload and oxidative stress in both A1 and A2 RAs, thereby alleviating WMI after SAH.
Conclusion:
EGCG-NPs attenuate SAH-induced WMI by inhibiting the iron overload-activated HO-1/S100A10 axis in RAs, representing a promising therapeutic strategy.
