Bergamot essential oil (BEO) is a rich source of terpenes, flavonoids, carotenes, and coumarins whose proposed physiological activities ranging from anti-inflammatory to antioxidant, from antiproliferative to neuromodulation. The present study was designed to explore whether BEO could attenuate heavy metal (Cd, Hg, and Pb) induced neurotoxicity in SH-SY5Y cells, utilized as a model system for brain cells. MTT, LDH and Calcein assays were used to examine the viability of the SH-SY5Y cells after exposure to heavy metals individually or in combination with BEO, as well as the effects of necrotic cell death, respectively. Furthermore, DCFH-DA assay was performed to determine whether BEO could protect SH-SY5Y from heavy metal-induced oxidative stress. Results allowed us to assess the capability of BEO to enhance the number of viable SH-SY5Y cells after exposure to heavy metal toxicity. Pre-treatment with BEO showed a considerable, concentration-dependent, cytoprotective effect, particularly against Cd induced toxicity. This effect was confirmed by reducing LDH release after the simultaneous cell treatment with Cd and BEO compared with Cd-treated cells. Furthermore, a significant, concentration-dependent decrease in ROS production, induced by H2O2 or heavy metals, was observed in the same model. Overall, the obtained results provide further insight into the protective role of BEO against heavy metal-induced neurotoxicity and oxidative stress.

Bergamot essential oil (BEO) provides cytoprotection in neuronal cells exposed to heavy metals.

Daniela Meleleo;
2024-01-01

Abstract

Bergamot essential oil (BEO) is a rich source of terpenes, flavonoids, carotenes, and coumarins whose proposed physiological activities ranging from anti-inflammatory to antioxidant, from antiproliferative to neuromodulation. The present study was designed to explore whether BEO could attenuate heavy metal (Cd, Hg, and Pb) induced neurotoxicity in SH-SY5Y cells, utilized as a model system for brain cells. MTT, LDH and Calcein assays were used to examine the viability of the SH-SY5Y cells after exposure to heavy metals individually or in combination with BEO, as well as the effects of necrotic cell death, respectively. Furthermore, DCFH-DA assay was performed to determine whether BEO could protect SH-SY5Y from heavy metal-induced oxidative stress. Results allowed us to assess the capability of BEO to enhance the number of viable SH-SY5Y cells after exposure to heavy metal toxicity. Pre-treatment with BEO showed a considerable, concentration-dependent, cytoprotective effect, particularly against Cd induced toxicity. This effect was confirmed by reducing LDH release after the simultaneous cell treatment with Cd and BEO compared with Cd-treated cells. Furthermore, a significant, concentration-dependent decrease in ROS production, induced by H2O2 or heavy metals, was observed in the same model. Overall, the obtained results provide further insight into the protective role of BEO against heavy metal-induced neurotoxicity and oxidative stress.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11369/458269
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