## 4 Discussion  
When DMN is injected intraperitoneally, the absorbed DMN from the visceral peritoneum drains into liver through the portal vein [24,25]. Finally, DMN induces diffuse micromodular cirrhosis with regenerative hepatocyte changes and bile duct proliferation [8,21,24]. Moreover, events such as increased mortality, destroyed hepatic parenchymal cell, and increased fibrosis in the DMN-induced rat model are similar to the progression in patients with cirrhosis [26]. In this study, the induced liver cirrhosis after intraperitoneal injection of DMN was indirectly confirmed by monitoring body weight and by serum biochemical assay, and the tissue condition was directly confirmed by histological analysis. Tissue conditions of DMN + AAE and DMN + Lac groups were significantly different from that of the DMN-only group. Unlike lactulose, AAE may have a different mechanism of reducing liver fibrosis because AAE has anti-inflammatory effects [15]. Although there was no significant difference in tissue conditions between the DMN + AAE and DMN + Lac groups, the DMN + AAE group showed a superior hepatic-protective effect on hepatic cirrhosis in the immunohistochemical analysis. After liver damage, HSCs transform into active contractile myofibroblasts and disturb the microcirculation [27,28]. Increased mobility and migration of HSCs contribute to the sinusoidal remodeling process and excessive function of HSCs results in pericytic dysfunction which is marked by phenotypic  
Figure 6: MR-based conductivity imaging and in vitro conductivity measurement of four experimental groups. (**a**) Anatomical MR image of phantom with four liver blocks; (**b**) electrical conductivity image of phantom; (**c**) bar graph showing comparison of measured conductivities from the imaging experiment; (**d**) line plot showing comparison of measured conductivities from an impedance analyzer. markers including \(\alpha\)-SMA [29; 30; 31]. In both the DMN + AAE and DMN + Lac groups, the level of \(\alpha\)-SMA expression and count of \(\alpha\)-SMA-positive cells were significantly lower than those of the DMN-only group. However, the DMN + AAE group showed a lower level of \(\alpha\)-SMA expression and decreased count of \(\alpha\)-SMA-positive cells than those of the DMN + Lac group which indicates superior ability to inhibit HSCs activation. Lactulose is often used to prevent hepatic encephalopathy by reducing the toxicity of ammonia in the blood rather than improving cirrhosis itself [32]. From the histological findings, the DMN + Lac group showed less hepatocyte injuries than the DMN-only group. This can be interpreted that lactulose may interfere with the proper induction of liver cirrhosis by DMN in the rat model. The mechanism for this result is not known; however, it can be speculated that lactulose reduced the level of the absorbed DMN in the mesenteric blood due to laxative effect including diarrhea via an increase in osmolality [27]. As a result, the degree of liver fibrosis in the DMN + Lac group was lower than that of the DMN-only group. [PERSON] et al. also reported that the degree of liver fibrosis was significantly reduced in DMN with lactulose treatment [8]. Chronic exposure of COX-2 and TNF-\(\alpha\) promotes inflammation and fibrosis, and ultimately leads to liver cirrhosis [8; 29; 33]. Compared with the DMN-only group, the level of COX-2 expression was significantly reduced in DMN + AAE and DMN + Lac groups which indicates AAE and Lac treatments ameliorated liver cirrhosis by reducing hepatic inflammation and fibrogenesis. In particular, the DMN + AAE group showed a lower level of COX-2 expression than that of the DMN + Lac group, which may indicate a superior inhibitory effect. [PERSON] et al. reported that curcumin could ameliorate liver cirrhosis via its anti-inflammatory effect and suppression of HSC activity, thereby attenuating fibrosis [8]. The results of curcumin in liver cirrhosis rat models were similar to those of AAE in this study [8].