The purpose of present study was to investigate the protective effect of silkworm excrement powder (SEP) on alcohol-induced hepatotoxicity in rats. Semisynthetic diet supplemented with SEP (3%, w/w) given to alcohol-feeding rats for 30 days, then blood and tissues were collected, processed and used for alcohol concentration mensuration, various biochemical estimations and histopathological examination. Chronic alcohol administration resulted in significantly increase in the activities of the clinically important liver marker enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyl transpeptidase (γ-GTP) and lactate dehydrogenase (LDH). Also, a highly significant increase in the blood alcohol level by alcohol treatment was observed. But alcohol-induced elevation of ALT and LDH levels markedly prevented and the level of blood alcohol decreased in SEP treated rats as compared to alcohol-administered control rats. SEP supplementation showed highly decreased the concentrations of total lipid, triglyceride and cholesterol in serum, as compared with alcohol treated control rats. Alcohol treatment induced the marked accumulation of large lipid droplets, hepatocytes necrosis and inflammation in the liver, but SEP administration attenuated to alcohol-induced accumulation of lipid droplets and hepatocyte necrosis. The results indicated that SEP may exert a protective effect against alcoholic hepatotoxicity through decreasing the activity of hepatic marker enzymes.

Hepatocellular carcinoma (HCC) is a representative inflammation-associated cancer and known to be the most frequent tumor. However, the preventive agents for hepatocarcinogenesis are unsatisfactorily identified. We investigated the protective effect of steamed and freeze-dried mature silkworm larval powder (SMSP) on diethylnitrosamine (DEN)-induced hepatotoxicity in mice and compared the effect of three silkworm varieties: white-jade, golden-silk, and light-green strains. The mice were fed with diet containing 0.1, 1, and 10 g/kg of three types of SMSP for two weeks while DEN (100 mg/kg, i.p.) was injected 18 h before the end of this experiment. Liver toxicity was determined as serum indicator, histopathological examination, and expression of inflammatory enzyme. Pretreatment with SMSP reduced necrotic and histopathological changes induced by DEN in the liver. The measurement of serum biochemical indicators showed that pretreatment with SMSP also decreased DEN-induced hepatotoxicity, the levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). In addition, SMSP inhibited the expressions of inflammatory enzymes, cyclooxygenase-2 and inducible nitric oxide synthase. White-jade SMSP showed the most effective hepatoprotective results against hepatotoxicity among the three silkworm strains used in this study. SMSP may have a protective effect against acute liver injury by inhibiting necrosis and inflammatory response in DEN-treated mice.