Beta-Caryophyllene, a Plant-Derived CB2 Receptor Agonist, Protects SH-SY5Y Cells from Cadmium-Induced Toxicity
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Published:2023-10-23
Issue:20
Volume:24
Page:15487
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ISSN:1422-0067
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Container-title:International Journal of Molecular Sciences
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language:en
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Short-container-title:IJMS
Author:
Mannino Federica1, Pallio Giovanni2ORCID, Imbesi Chiara1, Scarfone Alessandro1, Puzzolo Domenico2, Micali Antonio3, Freni José2ORCID, Squadrito Francesco1ORCID, Bitto Alessandra1, Minutoli Letteria1, Irrera Natasha1ORCID
Affiliation:
1. Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy 2. Department of Biomedical and Dental Sciences and Morphological and Functional Imaging, University of Messina, 98125 Messina, Italy 3. Department of Adult and Childhood Pathology “Gaetano Barresi”, University of Messina, 98125 Messina, Italy
Abstract
Cadmium (Cd) is a transition heavy metal that is able to accumulate in the central nervous system and may induce cell death through reactive oxygen species (ROS)-mediated mechanisms and inactivating the antioxidant processes, becoming an important risk factor for neurodegenerative diseases. The antioxidant effects of cannabinoid receptor modulation have been extensively described, and, in particular, β-Caryophyllene (BCP), a plant-derived cannabinoid 2 receptor (CB2R) agonist, not only showed significant antioxidant properties but also anti-inflammatory, analgesic, and neuroprotective effects. Therefore, the aim of the present study was to evaluate BCP effects in a model of Cd-induced toxicity in the neuroblastoma SH-SY5Y cell line used to reproduce Cd intoxication in humans. SH-SY5Y cells were pre-treated with BCP (25, 50, and 100 μM) for 24 h. The day after, cells were challenged with cadmium chloride (CdCl2; 10 μM) for 24 h to induce neuronal toxicity. CdCl2 increased ROS accumulation, and BCP treatment significantly reduced ROS production at concentrations of 50 and 100 μM. In addition, CdCl2 significantly decreased the protein level of nuclear factor erythroid 2–related factor 2 (Nrf2) compared to unstimulated cells; the treatment with BCP at a concentration of 50 μM markedly increased Nrf2 expression, thus confirming the BCP anti-oxidant effect. Moreover, BCP treatment preserved cells from death, regulated the apoptosis pathway, and showed a significant anti-inflammatory effect, thus reducing the pro-inflammatory cytokines increased by the CdCl2 challenge. The results indicated that BCP preserved neuronal damage induced by Cd and might represent a future candidate for protection in neurotoxic conditions.
Subject
Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis
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