Characterizing Eckol as a Therapeutic Aid: A Systematic Review

Manandhar, Bandana; Paudel, Pradeep; Seong, Su Hui; Jung, Hyun Ah; Choi, Jae Sue

Eckol isolated from Ecklonia cava had a cytoprotective effect against oxidative stress-induced cell damage in V79-4 cells. Eckol scavenged 2,2-diphenyl-1-picrylhydrazyl (DPPH) radicals, hydrogen peroxide (H 2 O 2 ), hydroxy radicals, and intracellular ROS, with dose-dependent quenching effects. At 30 µM, eckol demonstrated a 79% radical scavenging effect on intracellular ROS. Eckol also prevented lipid peroxidation (31% at 30 µM) in a thiobarbituric acid reactive substances (TBARS) assay, reducing cell death in V79-4 cells which was induced by H 2 O 2 . After eckol treatment, there was a decrease in nuclear fragmentation and the apoptotic sub-G 1 DNA content in V79-4 cells induced by H 2 O 2 . In addition, 30 µM eckol exhibited 47% and 43% ROS scavenging activity in cells damaged via serum starvation and γ-radiation, respectively. Eckol also influenced the activity of catalase by increasing it in a dose-dependent manner through the activation of phosphorylated ERK and NF-κB. Furthermore, eckol also increased the transcriptional activity of NF-κB. Hence, eckol is a capable of exhibiting cellular anti-oxidant activity and cytoprotection [43] .