[Polysaccharide from alleviates oxidative stress and hepatic fibrosis in -infected mice].

OBJECTIVE

To evaluate the role of polysaccharide from (PPI) in the improvement of oxidative stress, hepatic granuloma and hepatic fibrosis in in mice.

METHODS

The mouse model of schistosomiasis was established by cercariae infection via the abdomen. Balb/c mice were randomly assigned into 5 groups, including the healthy control group (Group A), infection control group (Group B), PPI treatment group (Group C), praziquantel treatment group (Group D) and PPI-praziquantel combination group (Group E), of 10 mice in each group. Each mouse in groups B, C, D and E was infected with (30 ± 2) cercariae. Then, mice in groups D and E were given praziquantel by gavage at a dose of 500 mg/kg for successive two days on day 42 post-infection, while mice in groups C and E were given PPI by gavage at a dose of 400 mg/kg for successive 30 days on day 42 post-infection. Histopathological changes of hepatic tissues were observed using hematoxylin-eosin (HE) staining, and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), laminin (LN) were determined, while the activities of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), glutathione reductase (GSH-R) and glutathione (GSH) were detected in Mouse liver homogenates. The expression of transforming growth factor-beta (TGF-β) and alpha-smooth muscle actin (α-SMA) was quantified in hepatic tissues using immunohistochemistry, and the and gene expression was quantified using quantitative real-time PCR (qPCR) assay.

RESULTS

Untreated mice presented typical pathological changes of schistosomal hepatic disorders, while PPI treatment effectively alleviated hepatic egg granulomas and collagen deposition. infection resulted in aggravation of hepatic lipid peroxidation, induction of oxidative stress, elevated serum MDA level and a reduction in the activity of GSH and antioxidant enzymes activities in mice. As compared to infected but untreated mice, PPI treatment suppressed hepatic lipid peroxidation, increased the GSH activity and restored the activity of antioxidant enzymes. In addition, PPI treatment inhibited the TGF-β signaling pathway and up-regulated the and gene expression.

CONCLUSIONS

PPI plays a critical role in the treatment of schistosomiasis-induced hepatic fibrosis. It may improve oxidative stress damages through up-regulating and gene expression, thereby suppressing the development of hepatic egg granulomas and hepatic fibrosis.