Ginsenoside Rb3 exerts protective properties against cigarette smoke extract-induced cell injury by inhibiting the p38 MAPK/NF-κB and TGF-ß1/VEGF pathways in fibroblasts and epithelial cells.
Biomed Pharmacother
; 108: 1751-1758, 2018 Dec.
Article
en En
| MEDLINE
| ID: mdl-30372878
ABSTRACT
Cigarette smoke causes many adverse effects such as inflammation, oxidative stress, and excessive accumulation of the extracellular matrix (ECM). Ginsenoside Rb3 has anti-inflammatory and anti-oxidative effects, which may contribute to delaying the injury caused by cigarette smoke. In this study, we used cigarette smoke extract (CSE) to establish cell injury models in WI-38 human fetal lung fibroblasts and 16HBE human bronchial epithelial cells. Our results showed that Rb3 protected against CSE-induced cytotoxicity in both cell lines. In addition, it significantly inhibited the secretion of inflammatory factors, such as interleukin-8 and tumor necrosis factor alpha, by inhibiting the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB). Moreover, Rb3 pre-treatment led to an increase in the levels of glutathione (GSH) and activities of superoxide dismutase, glutathione peroxidase (GSH-Px), and catalase to reduce the oxidative stress induced by CSE. Additionally, Rb3 decreased the levels of ECM proteins including collagen I (Col I), Col III, and elastin after CSE treatment by inhibiting the expression of transforming growth factor beta 1 (TGF-ß1)-induced vascular endothelial growth factor (VEGF). Our findings suggest that Rb3 prevented CSE-induced inflammation and oxidative stress as well as the excessive accumulation of ECM in WI-38 and 16HBE cells to protect against cell injury by inhibiting the p38 MAPK/NF-κB and TGF-ß1/VEGF pathways. The results of this study may be valuable for the development of Rb3 to combat the damage caused by cigarette smoke.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
FN-kappa B
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Ginsenósidos
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Factor A de Crecimiento Endotelial Vascular
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Proteínas Quinasas p38 Activadas por Mitógenos
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Células Epiteliales
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Factor de Crecimiento Transformador beta1
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Fibroblastos
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Fumar Cigarrillos
Tipo de estudio:
Prognostic_studies
Límite:
Humans
Idioma:
En
Año:
2018
Tipo del documento:
Article