알코올 급여 흰쥐에서 알코올성 간독성에 대한 누에배설물(silkworm excrement powder)의 영향을 검토하기 위하여 반합성 식이에 누에배설물을 3% (w/w) 수준으로 첨가하여 30일간 급여한 후 혈중 알코올 및 지질 농도, 간 기능 지표 효소 활성 및 간 조직 검사를 실시하였다. 임상생화학적으로 중요한 간 기능 지표 효소인 alanine aminotransferase (ALT), aspartate aminotransferase (AST), $gamma$-glutamyl transpeptidase ($gamma$-GTP) 및 lactate dehydrogenase (LDH) 활성이 알코올 대조군에서 증가하였다. 또한 혈중 알코올 농도도 알코올 섭취에 의해 증가하였다. 그러나 누에배설물 투여에 의해 혈중 ALT 및 LDH 활성은 현저하게 감소하였다. 혈중 중성지질, 콜레스테롤 농도는 알코올 대조군에 비해 누에배설물 투여에 의해 현저히 감소하였다. 또한 간 조직 검사에서 알코올 대조군에서 많은 지방적이 나타나 지방간이 확인되었으나 누에배설물 투여에 의해서는 지방적의 크기와 수가 많이 줄어드는 결과를 얻었다. 이상의 결과에서 누에배설물에 의한 알코올-유발 간독성의 개선효과는 간 조직의 임상생화학적 지표 효소의 활성 감소에 기인하는 것으로 나타났다.
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), $gamma$-glutamyl transpeptidase ($gamma$-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.
