Emodin ameliorates dopaminergic neuron loss in the MPP+ induced parkinson's disease model: significant inhibition of ferroptosis by activating UQCRC1 protein. (PubMed, Nat Prod Res) - May 9, 2025 - "Our experimental approach employed Erastin and MPP+-activated cellular systems to systematically evaluate this anthraquinone's therapeutic potential in counteracting iron-dependent programmed cell death mechanisms...These findings establish a novel regulatory axis linking UQCRC1 activation with ferroptosis inhibition, proposing emodin as a dual-function agent capable of both attenuating neuronal demise and modulating programmed cell death pathways. The pharmacological profile of emodin suggests clinical potential for intervening in ferroptosis-associated neurodegeneration."
Journal • CNS Disorders • Movement Disorders • Parkinson's Disease • UQCRC1
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Ayiguzhali Yusun; Chen-Ning Zhang; Hong-Mei Wan; Hua-Xian Chen; Mo Sun; Xu-Dong Ding
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