The data were analyzed using SPSS 13.0 software , and P 0.05 was considered statistically significant. RESULTS Emodin protected the liver against CCl4 induced injury and suppressed hepatic fibrogenesis in the rat model The effects of emodin on the protection of the liver from injury and fibrogenesis were initially evaluated by histological analyses. Representative views of liver sections are shown in Figure 1A. As shown in tissue sections stained with HE, compared with sections from livers in the vehicle controls , CCl4 caused prominent hepatic steatosis, necrosis, and formation of regenerative nodules and fibrotic septa between the nodules . Oral administration of emodin daily for 12 wk improved the state of steatosis with a significant reduction in the number of macro and microvesicular steatosis lesions, and it apparently suppressed hepatic fibrogenesis by reducing the thickness of bridging fibrotic septa . According to METAVIR scale, the degree of hepatic fibrosis increased markedly in the CCl4 group compared to the normal group, and decreased markedly in the emodin group compared to the CCl4 group . Taken together, emodin reduced hepatic fibrogenesis caused by chronic CCl4 intoxication.
Emodin reduced the content of hepatic hydroxyproline in the CCl4 rat model The efficacy of treatment with emodin on protection of the liver from fibrogenesis was further evaluated by using a quantitative method to determine the content of hepatic hydroxyproline in the rat model. Compared with the normal controls , the hepatic hydroxyproline PI3K Inhibitor content was significantly higher in rats injected with CCl4 . The hepatic hydroxyproline content was significantly reduced in rats treated with emodin at 20 mg kg . Emodin suppresses serum activities of ALT and AST in the CCl4 rat model Biochemical analyses of serum enzymes were performed to verify the role of emodin in the protection of the liver from injury. As shown in Figure 2, compared with those in the normal controls , the activities of serum ALT and AST were significantly higher in rats injected with CCl4 . The activities of serum ALT and AST were significantly reduced by administration of emodin .
These results demonstrated that emodin protected the liver against CCl4 induced injury. Emodin reduces HSC activation in the liver in the CCl4 rat model IHC and real time PCR experiments were performed to further evaluate the impact of emodin on regulating the SB-742457 cost selleck expression of SMA, the marker of activated HSC. Liver sections from each group were immunolabeled with antibodies against SMA. As shown in Figure 1B, as expected, few cells in the liver sections from the normal group were recognized by antibodies against SMA, suggesting few activated HSC in the normal livers in the vehicle control rats.