The inhibitory effect of chlorogenic acid on oxidative stress and apoptosis induced by PM2.5 in HaCaT keratinocytes.
J Biochem Mol Toxicol
; 38(9): e23806, 2024 Sep.
Article
en En
| MEDLINE
| ID: mdl-39148258
ABSTRACT
Exposure to fine particulate matter with an aerodynamic diameter of less than 2.5 µm (PM2.5) can cause oxidative damage and apoptosis in the human skin. Chlorogenic acid (CGA) is a bioactive polyphenolic compound with antioxidant, antifungal, and antiviral properties. The objective of this study was to identify the ameliorating impact of CGA that might protect human HaCaT cells against PM2.5. CGA significantly scavenged the reactive oxygen species (ROS) generated by PM2.5, attenuated oxidative cellular/organelle damage, mitochondrial membrane depolarization, and suppressed cytochrome c release into the cytosol. The application of CGA led to a reduction in the expression levels of Bcl-2-associated X protein, caspase-9, and caspase-3, while simultaneously increasing the expression of B-cell lymphoma 2. In addition, CGA was able to reverse the decrease in cell viability caused by PM2.5 via the inhibition of extracellular signal-regulated kinase (ERK). This effect was further confirmed by the use of the mitogen-activated protein kinase kinase inhibitor, which acted upstream of ERK. In conclusion, CGA protected keratinocytes from mitochondrial damage and apoptosis via ameliorating PM2.5-induced oxidative stress and ERK activation.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Queratinocitos
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Ácido Clorogénico
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Apoptosis
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Estrés Oxidativo
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Material Particulado
Límite:
Humans
Idioma:
En
Revista:
J Biochem Mol Toxicol
Asunto de la revista:
BIOLOGIA MOLECULAR
/
BIOQUIMICA
/
TOXICOLOGIA
Año:
2024
Tipo del documento:
Article
Pais de publicación:
Estados Unidos