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KMID : 1204320070230010059
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Laboratory Animal Research
2007 Volume.23 No. 1 p.59 ~ p.67
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Effects of Hwalgidan® on Hepatic Injury Induced by Carbon Tetrachloride in Rats
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Kim Eun-Ju
Kim Yun-Bae
Shin Sun-Hee
Jang Ja-Young
Park Dong-Sun
Park Jung-Hui
Choi Byong-Il
Jeon Jeong-Hee
Hwang Seok-Yeon
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Abstract
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Hepatoprotective effects of Hwalgidan® on both acute hepaotoxicity and chronic liver fibrosis and cirrhosis induced by carbon tetrachloride (CCI₄) were investigated in rats. In acute hepatotoxicity model, male Sprague-Dawley (SD) rats were injected intra peritoneally with CCI₄ at a dose of 1.0 ㎖/㎏ (20% in corn oil, 5 ㎖/㎏). Hwalgidan® was treated orally at doses of 100 or 500 ㎎/㎏ 4 hr and 30 min prior to as well as 4 hr and 20 hr after CCI₄ challenge. The rats were anesthesized with intraperitoneal injection of urethane (16.5% in saline, 6 ㎖/㎏) 4 hr following final Hwalgidan® treatment (24 hr after CCI₄ injection), and administered with bromosulphalein (SSP) solution (1% in saline, 2 ㎖/㎏). The blood concentration of SSP was quantified 21 and 46 min after intravenous administration. Also, complete blood counts and biochemical parameters related to hepatic injury in accordance with histopathological findings were analyzed. In chronic liver fibrosis and cirrhosis model, male SO rats were orally administered with CCI₄ at a dose of 1.0 ㎖/㎏ (50% in corn oil, 2 ㎖/㎏) for 33 days at 3-day intervals followed by 20-day recovery or daily Hwalgidan® (100 or 500 ㎎/㎏) treatment. Liver weights, blood biochemical parameters related to hepatic injury, histopathological findings in accordance with hydroxyproline concentrations were analyzed before and after Hwalgidan® treatment. Acute CCI₄ injection caused centrilobular congestion and hepatocytic degeneration, resulting in disintegration of hepatic cords, and thereby not only greatly increased blood biochemical markers related to hepatic injury and cholestasis, but also significantly delayed SSP clearance. Hwalgidan® (500 ㎎/㎏) markedly recovered the CCl₄-induced changes in blood biochemical values and SSP clearance, reducing hepatic lesion score to 1.72 from 2.50 in control group. Chronic exposure to CCI₄ reduced the body weight gain and induced overall hepatocytic fatty degeneration and extensive fibrosis, resulting in 5-fold increase in hyroxyproline level. Although Hwalgidan® did not affect the body and liver weights, it facilitated the recovery of blood biochemical values related to hepatic injury, hepatic lesions and fibrosis, and hydroxyproline contents. Taken together, it is suggested that Hwalgidan® might prevent acute hepatotoxicity and enhance the recovery of liver fibrosis and cirrhosis induced by CCI₄, and that Hwalgidan® or its ingredient could be a promising candidate for the prevention and treatment of hepatic disorders.
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KEYWORD
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Carbon tetrachloride(CCI₄), hepatotoxicity, fibrosis and cirrhosis, Hwangidan, hepatoprotection
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