This outcome manifested as a decrease in the cellular injury factor, which was closely correlated with biomarkers such as ALT and AST. The anti-oxidative effects of rhubarb anthraquinone derivatives, along with their hepatoprotective effects, have been reported. In XL-184 addition, a series of tannin-related compounds with strong antioxidant effects have been identified in RE. In a previous report, the antioxidant activities of rhubarb tannins were verified. Therefore, we believe that rhubarb tannins and anthraquinone derivatives may all contribute to the hepatoprotective effects of rhubarb against CCl4-induced liver damage. The hepatoprotective effect of rhubarb and its components has also been documented as antagonizing a-naphthylisothiocyanate – and concanavalin A – induced experimental liver injury. In a previous study, we found that free anthraquinones extracted from rhubarb, such as rhein and emodin, exhibited protective activity against ANIT-induced cholestatic liver injury by reducing the serum levels of glutamate-pyruvate transaminase, glutamic oxaloacetic transaminase and the serum total bilirubin, direct bilirubin, alkaline phosphatase, c-glutamyltransferase and total bile acids. These effects were markedly different from the effects on CCl4-induced liver injury. The morphological alterations induced by ANIT in rats, including the necrosis of hepatocytes and biliary epithelial cells, as well as neutrophil infiltration and sinusoid congestion, were also alleviated by concurrent intragastric administration of these free anthraquinones. Some clinical evidence has also revealed a hepatoprotective effect of rhubarb against infantile cholestatic hepatitis and acute icteric hepatitis. The protective effect against CCl4- induced liver damage reported in this study demonstrated only one aspect of the pharmacological potential of rhubarb to protect the liver. Although there is some evidence of the protective potential of this herb against liver injury due to multiple causes, the molecular mechanisms of this protection remain unclear. Rigorous clinical studies and in-depth experimental studies are needed to demonstrate rhubarb’s hepatoprotective effects and mechanisms of action. In our study, dose-dependent alterations of liver fibrosis associated with increases in the fibrosis factor were clearly observed in the rats in the normal groups. Although the occurrence of fibrosis of the liver tissues of normal rats that were treated with rhubarb has been reported infrequently, this phenomenon warrants further consideration. Elevation of TBIL, TP and GLO levels in serum have also been found in normal rat groups. These alterations usually occur along with hepatic impairment, indicating functional deterioration of the liver. Although the hepatoprotective effects of anthraquinone derivatives are well documented, it has also been reported that the total anthraquinone derivatives isolated from rhubarb show some hepatotoxic potential in rats in a six month-long experiment. Therefore, the dose-response relationship between rhubarb anthraquinones and liver health warrants further investigation.