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Curcumin protects against iron induced neurotoxicity in primary cortical neurons by attenuating necroptosis.
Dai, Min-Chao; Zhong, Zhi-Hong; Sun, Yu-Hao; Sun, Qing-Fang; Wang, Yong-Ting; Yang, Guo-Yuan; Bian, Liu-Guan.
Afiliação
  • Dai MC; Department of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025 China.
Neurosci Lett ; 536: 41-6, 2013 Mar 01.
Article em En | MEDLINE | ID: mdl-23328441
ABSTRACT
Necroptosis was reported as one backup way of programmed cell death when apoptosis was blocked, and the receptor interacting protein 1 was considered as the key necroptosis regulator protein. Here, we report the neuroprotective effects of curcumin which attenuates necroptosis. Primary cortical neurons were cultured and were injured by ferrous chloride, z.vad.fmk was applied to block apoptosis, curcumin was administrated to protect neurons, necrostatin-1 was applied to inhibit necroptosis if needed. Cell viability was measured by detecting lactate dehydrogenase activity in lysates of surviving cells, and assessed by cell counting kit-8. The expression of receptor interacting protein 1 was detected by immunoblot and immunofluorescence. Results showed that necroptosis mainly occurred in the concentrations of ferrous chloride ranging from 100 to 200µM, curcumin attenuated necroptosis in a dose-dependent manner. Furthermore, curcumin decreased expression of receptor interacting protein 1 in a dose- and time-dependent manner. Taken together, these findings suggest that curcumin protects against iron induced neurotoxicity in primary cortical neurons by attenuating necroptosis.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Córtex Cerebral / Fármacos Neuroprotetores / Sobrecarga de Ferro / Curcumina / Neurônios Idioma: En Ano de publicação: 2013 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Córtex Cerebral / Fármacos Neuroprotetores / Sobrecarga de Ferro / Curcumina / Neurônios Idioma: En Ano de publicação: 2013 Tipo de documento: Article