Oxidative Damage to BV2 Cells by Trichloroacetic Acid: Protective Role of Boron via the p53 Pathway / 生物医学与环境科学(英文)
Biomedical and Environmental Sciences
; (12): 657-662, 2022.
Article
em En
| WPRIM
| ID: wpr-939606
Biblioteca responsável:
WPRO
ABSTRACT
This study aimed to investigate the neurotoxicity induced by trichloroacetic acid (TCA) and the possible protective mechanisms of boron (B). Mouse BV2 cells were treated with TCA (0, 0.39, 0.78, 1.56, 3.12, 6.25, or 12.5 mmol/L) and B (0, 7.8, 15.6, 31.25, 62.5, 125, 500, or 1,000 mmol/L) for 3 h and 24 h, respectively. Then, reactive oxygen species, and supernatant proinflammatory cytokine and protein levels were analyzed after 24 h of combined exposure. Beyond the dose-dependent decrease in the cellular viability, it clearly increased after B supplementation ( P < 0.05). Moreover, B decreased oxidative damage, and significantly down-regulated IL-6 levels and up-regulated TNF-β production ( P < 0.05). B also decreased apoptosis via the p53 pathway. The present findings indicated that TCA may induce oxidative damage, whereas B mitigates these adverse effects by decreasing cell apoptosis.
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Base de dados:
WPRIM
Assunto principal:
Ácido Tricloroacético
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Boro
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Proteína Supressora de Tumor p53
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Espécies Reativas de Oxigênio
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Apoptose
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Estresse Oxidativo
Idioma:
En
Revista:
Biomedical and Environmental Sciences
Ano de publicação:
2022
Tipo de documento:
Article