This research demonstrates cardamomin's protective effects against oxidative damage in vitro and ischemic stroke in vivo, indicating it may support neuroprotection.
Ischemic stroke is characterized by disruption of cerebral blood flow, and the process of ischemic stroke produces excessive peroxides and consumes antioxidants, which is a trigger for neurological dysfunction and death. Cardamomin, a major constituent extracted from the stems and leaves of Amomum villosum , belongs to a chalcone with anti‐oxidative damage and neuroprotective activity. This study aimed to investigate the role and mechanism of cardamomin in oxidative damage and ischemic stroke. H 2 O 2 stimulation model of BV‐2 cells in vitro and permanent middle cerebral artery occlusion model of rats were used. CCK‐8 method, immunoblotting, immunofluorescence, comet assay, TTC staining, HE staining, and other methods were used to evaluate the protective effect of cardamomin on oxidative damage in vivo and in vitro. Our results demonstrated that cardamomin protected BV‐2 cells from oxidative damage caused by H 2 O 2 . Cardamomin inhibited oxidative stress by mediating NRF2 activation via the MEK/ERK pathway. Cardamomin mitigated oxeiptosis by inhibiting the dephosphorylation of AIFM1 Ser116. Cardamomin resisted parthanatos by preventing the nuclear translocation of AIFM1 and the disruption of DNA. In addition, cardamomin attenuated ischemic stroke in rats. In summary, this study reveals the antioxidant damage mechanism and preventive effect on cerebral ischemic stroke of cardamomin.
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Zhu et al. (2025) studied this question.
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