Hepatocyte damage, especially immunological liver injury, is a key process in the pathogenesis of hepatitis virus-induced liver diseases. The aim of this study was to investigate the protective effects of polyguluronate sulfate (PGS) against immunological liver damage. The results showed that PGS significantly reduced the H2O2-induced oxidative stress and increased the cell viability in HepG2 hepatocytes. PGS also suppressed the production of malondialdehyde (MDA), lactate dehydrogenase (LDH), TNF-α, and IL-6, while up-regulating the activity of SOD in HepG2 cells. Further, PGS (150 and 300mg/kg/day) significantly attenuated the elevation of serum glutamate pyruvate transaminase (ALT), aspartate aminotransferase (AST), total bilirubin (TBiL), in addition to liver MDA and NO levels in Con A-induced immunological liver injury within mice (P<0.05). Significant improvements of organ indexes (liver, spleen, and thymus) were observed in PGS-treated mice. PGS also significantly reduced the disorganization of hepatocytes and decreased the inflammatory cell infiltration caused by Con A treatment, suggesting that PGS was able to attenuate Con A-induced liver injury. In conclusion, PGS possesses significant hepatoprotective effects on immunological liver injury in vitro and in vivo, and this may be related to its antioxidant activities.
Keywords: Con A; Hepatoprotective effect; Liver injury; Oxidative stress; Polyguluronate sulfate.
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