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Curcumin protects neuronal-like cells against acrolein by restoring Akt and redox signaling pathways

Doggui, Sihem; Belkacemi, Abdenour; Paka, Ghislain Djiokeng; Perrotte, Morgane; Pi, Rongbiao; Ramassamy, Charles (2013). Curcumin protects neuronal-like cells against acrolein by restoring Akt and redox signaling pathways Molecular Nutrition and Food Research , vol. 57 , nº 9. p. 1660-1670. DOI: 10.1002/mnfr.201300130.

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Résumé

The aim of the present study was to examine the neuroprotective effect of curcumin against the toxicity induced by acrolein and to identify its cellular mechanisms and targets. Methods and results: Human neuroblastoma cells SK-N-SH were treated with acrolein. Curcumin, from 5 μM, was able to protect SK-N-SH cells against acrolein toxicity. The addition of curcumin restored the expression of γ-glutamylcysteine synthetase, reactive oxygen species, and reactive nitrogen species levels but had no effect on the decrease of glutathione (GSH) and on the elevation of protein carbonyls. Acrolein induced the activity of Nrf2, NF-κB, and Sirt1. These activations were prevented by the presence of curcumin. Acrolein also induced a decrease of the pAkt, which was counteracted by curcumin. To increase its solubility, we have encapsulated curcumin in a biodegradable poly(lactide-co-glycolide) based nanoparticulate formulation (Nps-Cur). Our results showed that 0.5 μM of Nps-Cur can protect neuronal cells challenged with acrolein while free curcumin was not able to display neuroprotection. Conclusion: Our results provided evidence that curcumin was able to protect SK-N-SH cells against acrolein toxicity. This protection is mediated through the antioxidant, the redox, and the survival regulated pathways by curcumin. Moreover, our results demonstrated that Nps-Cur had higher capacity than curcumin to protect SK-N-SH cells against acrolein.

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Mots-clés libres: Akt Alzheimer's disease Glutathione Nrf2 Sirtuins
Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 19 juin 2017 20:11
Dernière modification: 19 juin 2017 20:11
URI: http://espace.inrs.ca/id/eprint/2888

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