## 1 Introduction  
Liver cirrhosis is caused by the accumulation of long-term damage that leads to tissue degeneration and malfunction. The damage to liver tissues from alcohol, toxins, and certain drugs can result in inflammation, which refer to hepatitis. As a result, hepatic fibrosis occurs and progresses to cirrhosis over a long period of time [1]. The major phenomenon of liver fibrosis is the hepatic stellate cell (HSC) activation, which is a major source of extracellular matrix in liver fibrosis [2, 3]. Since HSCs express cytoplasmic alpha-smooth muscle actin (\(\alpha\)-SMA) intensely in response to liver damage, \(\alpha\)-SMA expression has been used to evaluate the amount of HSC activation and this correlates with the progress of liver fibrosis [4]. Although tissue changes in liver cirrhosis are known to be irreversible, several studies reported that liver fibrosis can be improved with appropriate treatments [5; 6]. In patients with liver cirrhosis, hepatic failure and hepatocellular carcinoma in advanced liver cirrhosis are known as the main causes of death [7]. Ameliorating liver fibrosis with effective treatments can prevent the progression to liver cirrhosis as well as reduce the incidence of hepatocellular carcinoma [5; 6; 8]. Several herbal extracts have been used for the treatment of liver cirrhosis [9; 10; 11; 12; 13]. For example, _Artemisia capillaries_ Thunb extracts decreased fibrogenic factor production, and specific _Artemisia capillaries_ Thunb fragments inhibited the proliferation of fibroblast [9; 14]. The Anemarrhenae rhizomes are also used to treat inflammatory diseases. A study reported that _Anemarrhena asphalodeoides_ extract (AAE) has an anti-inflammatory effect [15]. Specifically, mangiferin, the main constituent of AAE, inhibited the expression of pro-inflammatory cytokines and blocked the activation of nuclear factor \(\kappa\)-light-chain enhancer of activated B cells in lipopolysaccharide-stimulated peritoneal macrophages [15]. In addition, Timosaponin AIII, which is isolated from _Anemarrhena asphalodeoides_ Bunge is frequently used as an anti-pyretic, anti-inflammatory, anti-diabetic, and anti-depressive agent. The purified timosaponins and fractions of AAE containing timosaponins have various pharmacological effects which have a potential for improving inflammatory diseases as well as memory function of dementia patients [16]. Together with herbal extracts, many agents proven to have antifibrotic effects in vitro and in vivo animal models are being studied by clinical trials for the treatment of patients with liver fibrosis [2; 6]. The oral administration of lactulose with antibiotics used in clinical practice is helpful to inhibit intestinal endotoxin production in alcohol-fed animals and improve hepatic inflammation in a non-alcoholic steatohepatitis rat model [17]. However, oral administration of lactulose has side effects such as diarrhea and abdominal cramps [18]. Therefore, it may be appropriate to apply herbal medicines with a hepato-protective effect and fewer side effects for cirrhosis. However, in order to be used in clinical practice, its effectiveness should be objectively verified. Recently, magnetic-resonance (MR)-based electrical conductivity imaging showed a potential as an imaging tool to measure the therapeutic effects of herbal medicine [8]. The purpose of this study was to evaluate the ameliorating effects of AAE in an in vivo rat model with liver cirrhosis induced by intraperitoneal injection of dimethylnitrosamine (DMN). Rats were divided into four experimental groups such as normal liver, cirrhotic liver, cirrhotic liver with AAE treatment, and cirrhotic liver with lactulose treatment. The expression levels of \(\alpha\)-SMA in immunohistochemical analysis and levels of aminotransferase (AST), alanine aminotransferase (ALT), and albumin in blood were evaluated to the treatment effects in the four groups. In addition, the expression level of cyclooxygenase-2 (COX-2) was measured to evaluate the functionality of liver tissues among the groups.