Selected article for: "acute injury and addition possible"
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_123
    Snippet: An acute liver injury model in mice induced by carbon tetrachloride (CCl 4 ) was used to investigate the protective effects of eckol in addition to the possible mechanisms. The CCl 4 -induced rise in the serum levels of alanine transaminase (ALT) and (49.43 ± 16.03 U/L) and aspartate aminotransferase (AST) (63.21 ± 18.89 U/L) were suppressed by the pretreatment of eckol at doses of 0.5 and 1.0 mg/kg/day for 7 days with the amelioration of morph.....
    Document: An acute liver injury model in mice induced by carbon tetrachloride (CCl 4 ) was used to investigate the protective effects of eckol in addition to the possible mechanisms. The CCl 4 -induced rise in the serum levels of alanine transaminase (ALT) and (49.43 ± 16.03 U/L) and aspartate aminotransferase (AST) (63.21 ± 18.89 U/L) were suppressed by the pretreatment of eckol at doses of 0.5 and 1.0 mg/kg/day for 7 days with the amelioration of morphological liver injury. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) analysis revealed the decrease in the number of apoptotic hepatocytes in the eckol-treated group as compared to the CCl 4 model group. Eckol enhanced the expression of Bcl-2 and suppressed the expression of cleaved caspase-3, which reduced malondialdehyde formation, enhanced superoxide dismutase, glutathione peroxidase activity, and glutathione content, elevated TNF-α, and suppressed IL-1β and IL-6. Eckol also increased the level of IL-10, an anti-inflammatory cytokine with the recruitment of CD11c + dendritic cells into the liver tissue of CCl 4 -treated mice. Thus, inhibiton of apoptosis, oxidation, and inflammation including immune regulation are the multiple mechanisms related to protective effects of eckol [48] .

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