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The aqueous extract from Artemisia capillaris Thunb. inhibits lipopolysaccharide-induced inflammatory response through preventing NF-κB activation in human hepatoma cell line and rat liver
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2004
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Liver FibrosisImmunologyImmune RegulationOxidative StressLipopolysaccharide-induced Inflammatory ResponseInflammationPhytopharmacologyHepatotoxicityAeac PretreatmentLiver PhysiologyChronic InflammationHepatology InflammationPharmacologyInflammatory DiseaseDrug-induced Liver InjuryRat LiverAnti-inflammatoryHepatologyHepatitisArtemisia Capillaris ThunbMedicine
Artemisia capillaris Thunb. has been used for the remedy of liver diseases such as hepatitis, jaundice and fatty liver in traditional oriental medicine. However, despite extensive pharmacological studies, the molecular mechanism of the anti-inflammatory effect of Artemisia capillaris Thunb. has hardly been studied. In the present study, we investigated the pharmacological action mechanism on LPS-induced liver inflammation in HepG2 human hepatocarcinoma cells and rat liver. Aqueous extract from Artemisia capillaris Thunb. (AEAC) inhibits expression of inflammatory proteins including iNOS, COX-2 and TNF-alpha. Also, nuclear translocation of NF-kappaB and degradation of I-kappaBalpha are blocked by AEAC pretreatment. These results suggest that the inhibitory effect of AEAC on the expression of inflammatory proteins involves suppression of NF-kappaB activation.