Abstract
Phellinus gilvus (PG) is a widely used mushroom for health promotion. We studied the hepatoprotective effect of the polysaccharide aqueous extract of PG (PGP) against carbon tetrachloride (CCl4)-induced liver injury in rats. Sprague Dawley rats were divided into 5 groups: Normal control, CCl4 control, PGP 50, 100, and 200 mg/kg + CCl4. The levels of serum biochemical parameters, liver lipid peroxide and antioxidant enzymes, and histological appearances were evaluated. The CCl4-induced increments of alanine aminotransferase, asparate aminotransferase, and alkaline phosphatase levels in serum were significantly decreased by PGP-pretreatments. The PGP dose-dependently decreased hepatic malondialdehyde formations in CCl4-treatment groups. Hepatic antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) were elevated by PGP in CCl4-treatment groups. Histopathological evaluation of liver showed that the loss of hepatocytes, fatty changes, swelling and extensive necrosis of hepatocytes in centrilobular regions of the CCl4-treated rats were ameliorated by PGP pretreatment. The PGP has hepatoprotective and antioxidative effects in CCl4-induced liver injury of rat.
Highlights
Mushrooms have been valued as an important edible and medical resource
PGP pretreatment (100 and 200 mg/kg) significantly inhibited the elevation of ALT, AST, and alkaline phosphatase (ALP) levels by CCI4 (Fig. 1). These results suggest that PGP has liver cell regenerative effects and is able to stabilize membrane structures in hepatic injury
Under the present experimental single dose (1 ml/kg body weight), there were no changes in the other serum biochemical parameters at 24 hrs after CCI4 administration
Summary
Mushrooms have been valued as an important edible and medical resource. A number of bioactive materials have been identified in many mushroom species. Focus to evaluate the scientific basis for the traditional herbal medicines which are claimed to possess hepatoprotective activity. CCI4 is widely used in animal models to induce acute liver injury. Trichloromethyl radical, which is formed in the metabolism of CCI4 via the liver microsomal cytochrome P450 system, reacts rapidly with molecular oxygen to produce the trichloromethylperoxy radical. These radicals react with unsaturated fatty acids of phospholipids in the cell membrane, initiating lipid peroxidation in the liver cell (Recknagel et al, 1989). We examined the hepatoprotective effect of PGP pretreatment prior to CCI4 induced acute liver injury in the rat
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