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Curcumin-polydopamine nanoparticles alleviate ferroptosis by iron chelation and inhibition of oxidative stress damage.
Lei, Li; Yuan, Jiali; Yang, Qingqing; Tu, Qiuxia; Yu, Haijun; Chu, Liangzhao; Tang, Lei; Zhang, Chunlin.
Afiliação
  • Lei L; Engineering Research Center for Molecular Medicine, School of Basic Medical Science, Guizhou Medical University Guiyang 550025 China.
  • Yuan J; Department of Neurosurgery, The Affiliated Hospital of Guizhou Medical University Guiyang Guizhou China.
  • Yang Q; Engineering Research Center for Molecular Medicine, School of Basic Medical Science, Guizhou Medical University Guiyang 550025 China.
  • Tu Q; Guizhou Provincial Engineering Technology Research Center for Chemical Drug R&D, College of Pharmacy, Guizhou Medical University Guiyang 550025 China.
  • Yu H; Engineering Research Center for Molecular Medicine, School of Basic Medical Science, Guizhou Medical University Guiyang 550025 China.
  • Chu L; Center of Pharmaceutics, Shanghai Institute of Materia Medica, Chinese Academy of Sciences Shanghai 201203 China.
  • Tang L; Department of Neurosurgery, The Affiliated Hospital of Guizhou Medical University Guiyang Guizhou China.
  • Zhang C; Guizhou Provincial Engineering Technology Research Center for Chemical Drug R&D, College of Pharmacy, Guizhou Medical University Guiyang 550025 China.
RSC Adv ; 14(21): 14934-14941, 2024 May 02.
Article em En | MEDLINE | ID: mdl-38716098
ABSTRACT
Ferroptosis, characterized by elevated iron levels and lipid peroxidation (LPO), is a recently identified regulatory mechanism of cell death. Its substantial involvement in ischemic tissue injury, neurodegenerative disorders, and cancer positions ferroptosis inhibition as a promising strategy for managing these diverse diseases. In this study, we introduce curcumin-polydopamine nanoparticles (Cur-PDA NPs) as an innovative ferroptosis inhibitor. Cur-PDA NPs demonstrate remarkable efficacy in chelating both Fe2+ and Fe3+in vitro along with scavenging free radicals. Cur-PDA NPs were found to efficiently mitigate reactive oxygen species, reduce Fe2+ accumulation, suppress LPO, and rejuvenate mitochondrial function in PC12 cells. Thus, these NPs can act as potent therapeutic agents against ferroptosis, primarily via iron chelation and reduction of oxidative stress.

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article