D-Galactosamine (GaIN) induces acute hepatitis in experimental animals; this hepatitis has been shown to be suppressed by oral or intraperitoneal administration of modified arabinoxylan from rice bran (MGN—3) (also known as Lentin Plus 1000), and active low molecular fraction isolated from MGN-3 (LMW). We previously reported that this protective mechanism is mediated in part by downregulation of interleukin-18 (IL-18), The present study shows for the Hrst time that nuclear factor- κB (NF- κB), mitogen-activated protein kinase (MAPK) and CD14 are involved in the suppressive action of LMW on GaIN-induced hepatitis Wistar rats (aged 4 weeks, SLC) were intraperitoneally treated with either MGN—3 or LMW. Then, rats were given GaIN at 400 mg/kg at 1 h after the initial treatment, The serum activity of transaminases (ALT and AST) was significantly higher after GaIN treatment: these changes were attenuated by MGN—3 and LMW.

Furthermore, LMW abrogated inhibitor of κB kinase (I κB) degradation induced by GaIN, and this was associated with the inhibition of NF κB activation. Moreover, phosphorylated stress-activated protein kinase/c-jun N-terminal kinase (JNK) protein expression in the liver after GaIN treatment was significantly higher, and LMW reduced this increase. We also found that GaIN treatment induced TLR4 and CD14 mRNA expression, and LMW significantly inhibited CD14 mRNA expression. These results suggest that the suppressive effects of LMW on GaIN—induced hepatitis are possibly related to inhibition of NF- κB,NK phosphorylation and CD14 expression.