The complex ethiology of neurodegenerative diseases suggests a combined approach to their prevention, targeting neuroinflammation and stimulating the cellular degradation systems such as autophagy. Many pro-inflammatory molecules are ligands of Toll-like receptors, activators of autophagic pathway, thus autophagy might be prompted by these stimuli in astrocytes, whose key role during inflammation is well established. Sulforaphane (SF), an isothiocyanate of Brassica vegetables, has generated a great interest for its neuroprotective properties. We thus examined whether inflammation triggers autophagy in astrocytes and the contribution of SF in modulating the cellular and molecular mechanisms underpinning neuroinflammatory effects. We observed that astrocytes react with autophagy to inflammation to prevent death, and that SF treatment is able to mimic this response. Further experiments are now required in order to gain insight into the mechanism underlying inflammation-induced autophagy and the effect of SF.

Targeting autophagy in inflammed cortical astrocytes: novel protective strategies for nutraceutical compounds.

MOTORI, ELISA;ANGELONI, CRISTINA;LEONCINI, EMANUELA;MALAGUTI, MARCO;FABBRI, DANIELE;BIAGI, PIERLUIGI;HRELIA, SILVANA
2010

Abstract

The complex ethiology of neurodegenerative diseases suggests a combined approach to their prevention, targeting neuroinflammation and stimulating the cellular degradation systems such as autophagy. Many pro-inflammatory molecules are ligands of Toll-like receptors, activators of autophagic pathway, thus autophagy might be prompted by these stimuli in astrocytes, whose key role during inflammation is well established. Sulforaphane (SF), an isothiocyanate of Brassica vegetables, has generated a great interest for its neuroprotective properties. We thus examined whether inflammation triggers autophagy in astrocytes and the contribution of SF in modulating the cellular and molecular mechanisms underpinning neuroinflammatory effects. We observed that astrocytes react with autophagy to inflammation to prevent death, and that SF treatment is able to mimic this response. Further experiments are now required in order to gain insight into the mechanism underlying inflammation-induced autophagy and the effect of SF.
55th National Meeting of the Italian Society of Biochemistry and Molecular Biology (SIB)-Congress Abstracts
37
37
E. Motori; C. Angeloni; E. Leoncini; M. Malaguti; D. Fabbri; P.L. Biagi; S. Hrelia.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/91238
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