Characterizing Eckol as a Therapeutic Aid: A Systematic Review

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

To further support the radioprotective potential of eckol, E. cava was evaluated to determine its cyto-and histoprotective ability in lymphocytes and the intestine against damage induced by whole body irradiation (WBI) in vivo. To assess whether the effectiveness of eckol in inhibiting DNA damage was accountable to apoptotic changes, the nuclear morphology of lymphocytes was assessed in irradiated mice as peripheral blood lymphocytes are easily harmed by ionizing radiation. The number of apoptotic nuclei was reduced dramatically in the eckol treated group in comparison with the irradiated control group (9.95 ± 0.50% versus 14.85 ± 0.39%). Hence, the viability of peripheral blood lymphocyte was protected by inhibiting apoptotic cell death induced by ionizing radiation in vivo. The frequency of apoptotic fragments in crypt cells was reduced in the eckol-treated group by 16 .63% compared to the untreated group (4.51 ± 0.30%) after 24 h of WBI treatment revealing the ability of eckol to protect intestinal crypt cells from radiation-induced apoptosis. The increase in the expression level of p53 and Bax, commonly seen after WBI, was also reduced by eckol with the induction in the expression level of Bcl-2, which is involved in apoptosis and DNA repair. In those ways, eckol treatment modulated the immunohistochemical localization and magnitude of apoptosis-related proteins in jejunal crypt cells. Therefore, eckol administration could provide great benefits for cancer patients by effectively preventing the apoptosis of peripheral blood lymphocytes and intestinal crypt cells induced by radiation [62] . Furthermore, eckol pre-treatment scavenged ROS in γ-irradiated V79-4 cells and protected against DNA damage by decreasing 8-OHdG adduct of DNA, a biomarker of oxidative stress. Eckol also decreased the lipid peroxidation in the γ-irradiated V79-4 cells. The apoptosis induced by γ-irradiation was also decreased in eckol (10 µg/ml) pre-treated cells with a decrease in DNA fragmentation. An increase in Bcl-2 expression and a decrease of Bax expression in γ-ray irradiated cells treated with eckol further inhibiting the caspase-dependent pathway via mitochondria. The SEK1-JNK-AP-1 is the major pathway that is suppressed by eckol for decreasing the γ-ray irradiation-induced apoptosis [65] .