Fucoidan alleviates microcystin-LR-induced hepatic, renal, and cardiac oxidative stress and inflammatory injuries in mice
Résumé
Fucoidans (FUCs) are sulfated polysaccharides that have a wide range of bioactivities. The current study was designed to
evaluate the antioxidant potential of FUC against microcystin-LR (MC-LR)-induced toxicity. Five mice groups (n = 8) were
used. Group 1 received saline, Group 2 received oral FUC 100 mg/kg/day for 21 days, Group 3 received i.p. MC-LR 10 μg/kg/
day for 14 days, Group 4 received MC-LR plus FUC 50 mg/kg/day, and Group 5 received MC-LR plus FUC 100 mg/kg/day. The
present study showed that MC-LR administration was associated with significant increases (p < 0.01) in serum concentrations of
hepatic (aspartate transferase, alanine transferase, and alkaline phosphatase), renal (urea and creatinine), and cardiac (creatine
kinase and CK-MB) injury biomarkers, as well as serum lactate dehydrogenase, cholesterol, and pro-inflammatory cytokines
(interleukins-1β and 6, and tumor necrosis factor-α), compared with the control group. Further, MC-LR-intoxicated mice
exhibited significantly higher (p < 0.01) hepatic, renal, and cardiac tissue levels of malondialdehyde and nitric oxide, as well
as lower tissue levels of reduced glutathione and activities of glutathione peroxidase, superoxide dismutase, and catalase enzymes
in comparison with control mice. Treatment by FUC significantly ameliorated all the above-mentioned alterations in a dosedependent manner with frequent restoration of the normal ranges in the FUC 100 mg/kg/day dose group. Moreover, treatment by
FUC alone at 100 mg/kg/day was not associated with significant negative alterations in the assessed biochemical parameters,
highlighting its safety at this dose. In conclusion, treatment by FUC significantly ameliorated organ injury, induced by MC-LR in
mouse hepatic, renal, and cardiac tissues.