Cannabidiol Protects Dopaminergic Neuronal Cells from Cadmium

Jacopo Junio Valerio Branca, Gabriele Morucci, Matteo Becatti, Donatello Carrino, Carla Ghelardini, Massimo Gulisano, Lorenzo Di Cesare Mannelli and Alessandra Pacini
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Jacopo Junio Valerio Branca: Department of Experimental and Clinical Medicine, Histology and Anatomy Section, University of Firenze, 50134 Firenze, Italy
Gabriele Morucci: Department of Experimental and Clinical Medicine, Histology and Anatomy Section, University of Firenze, 50134 Firenze, Italy
Matteo Becatti: Department of Experimental and Clinical Biomedical Sciences “Mario Serio”, University of Firenze, 50134 Firenze, Italy
Donatello Carrino: Department of Experimental and Clinical Medicine, Histology and Anatomy Section, University of Firenze, 50134 Firenze, Italy
Carla Ghelardini: Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Pharmacology and Toxicology Section, University of Firenze, 50139 Firenze, Italy
Massimo Gulisano: Department of Experimental and Clinical Medicine, Histology and Anatomy Section, University of Firenze, 50134 Firenze, Italy
Lorenzo Di Cesare Mannelli: Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Pharmacology and Toxicology Section, University of Firenze, 50139 Firenze, Italy
Alessandra Pacini: Department of Experimental and Clinical Medicine, Histology and Anatomy Section, University of Firenze, 50134 Firenze, Italy

IJERPH, 2019, vol. 16, issue 22, 1-17

Abstract: The protective effect of cannabidiol (CBD), the non-psychoactive component of Cannabis sativa , against neuronal toxicity induced by cadmium chloride (CdCl 2 10 μM) was investigated in a retinoic acid (RA)-differentiated SH-SY5Y neuroblastoma cell line. CBD (1 μM) was applied 24 h before and removed during cadmium (Cd) treatment. In differentiated neuronal cells, CBD significantly reduced the Cd-dependent decrease of cell viability, and the rapid reactive oxygen species (ROS) increase. CBD significantly prevented the endoplasmic reticulum (ER) stress (GRP78 increase) and the subcellular distribution of the cytochrome C, as well as the overexpression of the pro-apoptotic protein BAX. Immunocytochemical analysis as well as quantitative protein evaluation by western blotting revealed that CBD partially counteracted the depletion of the growth associated protein 43 (GAP43) and of the neuronal specific class III β-tubulin (β3 tubulin) induced by Cd treatment. These data showed that Cd-induced neuronal injury was ameliorated by CBD treatment and it was concluded that CBD may represent a potential option to protect neuronal cells from the detrimental effects of Cd toxicity.

Keywords: cadmium; cannabidiol; ER stress; ROS; SH-SY5Y; neurotoxicity (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2019
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