Resumen
Anemarrhena asphodeloides extract (AAE) has been used for the treatment of inflammatory diseases and its anti-inflammatory effects have been reported. In this feasibility study, the hepato-protective effect of AAE was evaluated in a rat liver cirrhosis model by a combination of biochemical analysis and electrical tissue conductivity. Liver cirrhosis was induced by dimethylnitrosamine (DMN) injection. A total of 32 Sprague?Dawley rats were divided into four groups such as normal liver, cirrhotic liver, cirrhotic liver with AAE treatment, and cirrhotic liver with lactulose treatment. Effects of AAE were compared with those of lactulose. Cirrhotic liver with both AAE and lactulose treatments showed increased body weight, decreased levels of aspartate aminotransferase and alanine aminotransferase, and increased albumin level compared with cirrhotic liver (p < 0.05). The expression levels of a-smooth muscle actin (a-SMA) and cyclooxygenase-2 (COX-2) in immunohistochemical analysis showed reduced fibrosis and inflammatory response in both AAE and lactulose treatments compared with cirrhotic liver (p < 0.05). The levels of AAE treatment were relatively lower than those of lactulose. The western blot analysis of a-SMA and COX-2 protein in both AAE and lactulose treatments was similar to that of normal liver. When comparing electrical conductivity to normal liver, difference in conductivity was 21.2%, 11.5%, and 7.7% in cirrhotic liver, lactulose treatment, and AAE treatment, respectively. These results suggest that the anti-inflammatory effect of AAE may delay or prevent the progress from liver fibrosis to cirrhosis. In summary, a more precise analysis of tissue conditions following the induction of liver cirrhosis was possible by combining electrical tissue conductivity with conventional biochemical analysis.