Objective: To investigate the change of selenoprotein S1 (SEPS1) hepatic expression in septic mouse induced by LPS attack.
Methods: The septic murine model induced by LPS attack was established. Ten mice were randomly selected as control group from 84 BALB/c mice and others as septic group. The mice were sacrificed after anesthesia in control group and 10 mg/kg LPS was injected intraperitoneally into septic group mice. Liver and blood samples were taken at 6, 12, 24, 48, 72 and 96 h after LPS injection. Ten mice were randomly selected at each time point. The levels of blood ALT, AST, LDH and liver IL-6, TNF-α were detected. And the SEPS1 expression was simultaneously detected by Western blot.
Results: There was liver damage in septic group compared with normal control group. The levels of ALT, AST and LDH markedly increased. And all peaked at 24 h. The levels were (99 ± 11), (299 ± 48) and (1523 ± 131) U/L respectively (versus level at zero hour, P < 0.05). Then there was a gradual decrease and the pre-damage levels were restored during 24-72 h. The levels of IL-6 and TNF-α also markedly increased. The damage deteriorated rapidly and peaked at 48 h. The levels were (30,325 ± 17,901) and (36,509 ± 20,794) ng/L respectively [versus level at zero hour (23,802 ± 11,150), (29,799 ± 8239) ng/L, P < 0.05]. Western blot showed that SEPS1 protein expression markedly increased simultaneously in liver of septic mouse. And the peak value was reached at 24 h post-injury. Then there was a gradual decrease and normal level returned at 72 h. Immunohistochemical results showed that SEPS1 protein expression in liver of septic mouse also markedly increased. And the peak value was reached at 24 h post-injury. Pathologic results showed that liver lesion was apparent in septic mouse and it was the worst during 6-12 h.
Conclusion: Liver damage to different extents may be induced by LPS attack in septic mouse. The levels of IL-6 and TNF-α markedly increase. The SEPS1 protein expression in liver of septic mouse is also markedly elevated. And it peaks at 24 h post-injury and returns to normal at 72 h.
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FASEB J
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Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
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