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The protective effect of rossicaside B, the major phenylpropanoid glycoside from Boschniakia rossica, on CCl 4 -induced hepatotoxicity and the mechanisms underlying its protective effect were investigated. The mice were administered orally with rossicaside B (100 or 200 mg ⁄ kg of body weight) 48, 24 and 1 hr before CCl 4 (0.5 ml ⁄ kg of body weight) administration. The CCl 4 challenge caused a marked increase in the levels of serum aspartate aminotransferase, alanine aminotransferase and of tumour necrosis factor-a, and propagated lipid peroxidation with a concomitant reduction in reduced glutathione (GSH) and antioxidative enzyme activities in the liver. The administration of rossicaside B to CCl 4 -treated mice not only decreased the serum toxicity marker enzymes and TNF-a but also reduced hepatic oxidative stress, as demonstrated by decreased lipid hydroperoxide and thiobarbituric acid-reactive substance concentrations, combined with elevated GSH content and antioxidative enzyme activities in the liver tissues. Furthermore, the contents of hepatic nitrite, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and haem oxygenase-1 (HO-1) were elevated after CCl 4 treatment while the cytochrome P450 2E1 (CYP2E1)-specific monooxygenase activity was suppressed. Rossicaside B treatment inhibited the formation of liver nitrite, reduced the over-expression of iNOS and COX-2 proteins, but increased the CYP2E1 function compared with the CCl 4 -treated mice. However, the protein expression of HO-1 was further elevated by rossicaside B treatment. The results demonstrate that rossicaside B provides a protective action on CCl 4 -induced acute hepatic injury, which may be related to its antioxidative activity, suppressed inflammatory responses, induced HO-1 expression and improved CYP2E1 function in the liver.

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