Protection against Oxidative Stress-Induced Apoptosis by Fermented Sea Tangle (<i>Laminaria japonica</i> Aresch) in Osteoblastic MC3T3-E1 Cells through Activation of Nrf2 Signaling Pathway
The purpose of the present study was to explore the efficacy of fermented extract of sea tangle (<i>Laminaria japonica</i> Aresch, FST) with <i>Lactobacillus brevis</i> on DNA damage and apoptosis in hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-stimu...
Guardado en:
| Autores principales: | , , , , , , , , , , , , , |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
MDPI AG
2021
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/1503b3e472314af1b6ca09109f9a3019 |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| Sumario: | The purpose of the present study was to explore the efficacy of fermented extract of sea tangle (<i>Laminaria japonica</i> Aresch, FST) with <i>Lactobacillus brevis</i> on DNA damage and apoptosis in hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-stimulated osteoblastic MC3T3-E1 cells and clarify related signaling pathways. Our results showed that exposure to FST significantly improved cell viability, inhibited apoptosis, and suppressed the generation of reactive oxygen species (ROS) in H<sub>2</sub>O<sub>2</sub>-stimulated cells. In addition, H<sub>2</sub>O<sub>2</sub> triggered DNA damage in MC3T3-E1 cells was markedly attenuated by FST pretreatment. Moreover, H<sub>2</sub>O<sub>2</sub>-induced mitochondrial dysfunctions associated with apoptotic events, including loss of mitochondrial membrane potential (MMP), decreased Bcl-2/Bcl-2 associated x-protein (Bax) ratio, and cytosolic release of cytochrome <i>c</i>, were reduced in the presence of FST. FST also diminished H<sub>2</sub>O<sub>2</sub>-induced activation of caspase-3, which was associated with the ability of FST to protect the degradation of poly (ADP-ribose) polymerase. Furthermore, FST notably enhanced nuclear translocation and phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2) in the presence of H<sub>2</sub>O<sub>2</sub> with concomitant upregulation of heme oxygenase-1 (HO-1) expression. However, artificial blockade of this pathway by the HO-1 inhibitor, zinc protoporphyrin IX, greatly abolished the protective effect of FST against H<sub>2</sub>O<sub>2</sub>-induced MC3T3-E1 cell injury. Taken together, these results demonstrate that FST could protect MC3T3-E1 cells from H<sub>2</sub>O<sub>2</sub>-induced damage by maintaining mitochondrial function while eliminating ROS along with activation of the Nrf2/HO-1 antioxidant pathway. |
|---|