Author: Manandhar, Bandana; Paudel, Pradeep; Seong, Su Hui; Jung, Hyun Ah; Choi, Jae Sue
Title: Characterizing Eckol as a Therapeutic Aid: A Systematic Review Document date: 2019_6_18
ID: 0dpv85od_113
Snippet: Similarly, there was an induction of heme oxygenase (HO)-1 mRNA and protein expression in the Chinese hamster lung fibroblast (V79-4) cells in a concentration-and time-dependent manner, due to eckol, which resulted in high HO-1 activity. Enhancement of the phosphorylated form, nuclear translocation, antioxidant response element (ARE)-binding, and transcriptional activity of Nrf2 was observed in V79-4 cells upon exposure to 10 µg/mL of eckol. Fur.....
Document: Similarly, there was an induction of heme oxygenase (HO)-1 mRNA and protein expression in the Chinese hamster lung fibroblast (V79-4) cells in a concentration-and time-dependent manner, due to eckol, which resulted in high HO-1 activity. Enhancement of the phosphorylated form, nuclear translocation, antioxidant response element (ARE)-binding, and transcriptional activity of Nrf2 was observed in V79-4 cells upon exposure to 10 µg/mL of eckol. Furthermore, Nrf2 mediated the eckol-induced activation of the HO-1 promoter. The Nrf2 activation and induction of HO-1 expression were due to the contribution of the extracellular related kinase (Erk) and phosphoinositide 3-kinase/protein kinase B (PI3K/PKB). To further assess the likeliness of the cytoprotective activity of eckol due to HO-1 induction, the V79-4 cells were pretreated with HO-1 inhibitor zinc protoporphyrin (10 µM) and transfected with HO-1 siRNA (10-50 nM) and Nrf2 siRNA (10-50 nM). All of them markedly reduced the cytoprotective effect of eckol against H 2 O 2 -induced cell damage suggesting the involvement of Nrf2 transcription factor in eckol-mediated HO-1 induction. Additionally, the cytoprotective effect of eckol was reduced by U0126 (an inhibitor of ERK kinase) (10 nM) and LY294002 (an inhibitor of PI3K) (5 µM). Therefore, eckol has the ability to attenuate oxidative stress-induced cell death through Nrf2-mediated HO-1 activation via Erk and PI3K/Akt signaling [42] .
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