Hepatoprotective Effects of Polysaccharides from Selenium-Enriched Pyracantha fortuneana on Mice Liver Injury

Pyracantha fortuneana (Maxim.) Li (P. fortuneana), an Asian species of firethorn of family Rosaceae abundantly distributed in several regions in China, has been used as a traditional Chinese medicine. We have previously reported that polysaccharides extracted from P. fortuneana lowered the oxidative stress and inhibited the inflammatory responses in mice. Other studies recently reported that proanthocyanidins from P. fortuneana promoted cellular antioxidant activity of quercetin in HepG2 cell. Our present study aims to determine the hepatoprotective effects of Selenium enriched P. fortuneana polysaccharides (Se-PFPs) against carbon tetrachloride (CCl4)-induced liver injury in a mouse model. Mice were randomly grouped into five groups, 10 mice per group: (A) normal control group; (B) CCl4 group; (C) biphenyldicarboxylate pills (BP) + CCl4 group; (D) Se-PFP(I) + CCl4 group; and (E) Se-PFP(Ⅱ) + CCl4 group. Mice in A group were given olive oil (2 ml/kg body weight (b.w.)) by intraperitoneal injection (I.P.) twice a week for 5 weeks. Mice in groups B, C, D and E were given CCl4 (2 ml/kg b.w., 30% in olive oil) by I.P. injection twice a week for 5 weeks. Mice in C, D and E groups were also given supplements containing BP (200mg/kg), Se-PFP(I) (200mg/kg) and Se-PFP(II) (400mg/kg), respectively. After dosing for 5 weeks, serum and liver enzymes, lipid profile, and lipid peroxidation levels were measured. Real time (RT)-PCR and western blot were used to determine gene expression levels. CCl4 group displayed remarkable elevation in the levels of alanine transferase (ALT), aspartate transaminase (AST), H2O2, thiobarbituric acid reactive substances (TBAR), lactic dehydrogenase (LDH), lipid profile, malondialdehyde (MDA) and a remarkable decrease in glutathione peroxidase (GPx), glutathione (GSH), catalase (CAT), paraoxonase-1 (PON1), paraoxonase-3 (PON3), and superoxide dismutase (SOD). Similar to BP treatment, supplementation of mice with Se-PFPs resulted in reversal of biochemical indicators and expression levels of those genes caused by CCl4. Our study indicates that Se-PFP administration is effective in attenuating CCl4-induced liver injury. The mechanism underlying this effect may be attributed to the reduction of oxidative stress and inflammation in liver by Se-PFPs through up-regulation of the antioxidant system. Our study suggests that Se-PFP might be a potential dietary agent in the prevention of hepatic damage.