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This study investigates the neuroprotective effect of a combination of two natural anthraquinones, rhein and emodin, against ferroptosis, focusing on the mitochondrial complex III subunit UQCRC1. Using network pharmacology and experimental validation in erastin\/MPP\n                    <jats:sup>+<\/jats:sup>\n                    \u2010induced PC12 cells, we found that the optimal rhein\u2013emodin combination potently inhibited ferroptotic cell death. This effect was associated with restored mitochondrial function, reduced lipid peroxidation, and the coordinated regulation of ferroptosis\u2010related proteins, including the upregulation of GPX4 and FTH and downregulation of ACSL4. Crucially, the co\u2010treatment markedly activated UQCRC1 expression. Furthermore, UQCRC1 knockdown abolished these anti\u2010ferroptotic effects, establishing it as an essential mediator. Our findings demonstrate that the rhein\u2013emodin combination attenuates ferroptosis primarily through UQCRC1 activation, highlighting its therapeutic promise and identifying UQCRC1 as a novel regulatory node for PD intervention.\n                  <\/jats:p>","DOI":"10.1002\/cbdv.202502053","type":"journal-article","created":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T16:52:11Z","timestamp":1773679931000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Rhein\u2013Emodin Combination Activates UQCRC1 to Attenuate MPP\n                    <sup>+<\/sup>\n                    \u2010Induced Ferroptosis in Dopaminergic Neurons"],"prefix":"10.1002","volume":"23","author":[{"given":"Ayiguzhali","family":"Yusun","sequence":"first","affiliation":[{"name":"Department of Rehabilitation Medicine Postgraduate Union Training Base of Xiangyang No.1 People's Hospital School of Medicine Wuhan University of Science and 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