Effects of emodin on treating murine nonalcoholic fatty liver induced by high caloric laboratory chaw

Abstract

Aim: To investigate the effects of emodin on the treatment of non-alcoholic fatty liver in rats induced by high caloric laboratory chaw.

Methods: Non-alcoholic fatty liver model was successfully established by feeding with high caloric laboratory chaw for 12 wk. Then the model rats were randomly divided into 3 groups, namely model control group, emodin group and dietary treatment group. The rats in emodin group were given emodin at dose of 40 mg/(kg x d) while animals in other groups were given distilled water of the same volume. The rats in model control group were fed with high caloric laboratory chaw while animals in other groups were fed with normal diet. Four weeks later, liver index (liver/body weight ratio), serum activities of liver-associated enzymes, blood lipid, fasting blood glucose, fasting plasma insulin, HOMA insulin resistance index (HOMA-IR), hepatic triglyceride content and histology features of all groups were assayed. The expression of hepatic peroxisomal proliferator activated receptor (PPAR) gamma was determined by RT-PCR.

Results: The body weight, liver index, serum activities of alanine aminotransferase (ALT), blood lipid, hepatic triglyceride content of model control group were significantly elevated, with moderate to severe hepatocyte steatosis. The expression of hepatic PPAR gamma mRNA was obviously reduced in model control group. Compared with model control group, the body weight, liver index, serum activities of ALT, blood lipids and hepatic triglyceride of emodin group significantly decreased and hepatic histology display was also greatly improved. Meanwhile, the expression of hepatic PPAR gamma mRNA was elevated. However, high serum activities of ALT and hyperlipidemia were persisted in dietary treatment group although liver index was decreased and liver histology was somewhat improved.

Conclusion: It is suggested that emodin might be effective in the treatment of non-alcoholic fatty liver in rats. Its therapeutic mechanism could be associated with increasing the expression of hepatic PPAR gamma mRNA.

Figure 1

Body weight and liver index changes among four groups. A: Comparison of murine body weight among relevant groups. ^aP<0.05 vs normal group, ^cP<0.05 vs model control group; B: Comparison of liver index among relevant groups. ^bP<0.01 vs normal group, ^dP<0.01 vs model control group.

Figure 2

Hepatic enzyme activity, blood lipids levels and hepatic TG contents among four groups. A: Comparison of serum ALT and AST activities among relevant groups. ^aP<0.05 vs normal group, ^cP<0.05 vs model control group; B: Comparison of serum TC and TG levels among relevant groups. ^aP<0.05 vs normal group, ^bP<0.01 vs normal group, ^cP<0.05 vs model control group, ^dP<0.01 vs model control group; C: Comparison of hepatic TG contents among relevant groups. ^bP<0.01 vs normal group, ^cP<0.05 vs model control group.

Figure 3

The expression of PPAR-gamma mRNA in murine liver tissues. M: marker. Lane 1: normal group; lane 2: model control group; lane 3: emodin group; lane 4: dietary group.

Figure 4

Hepatopathological manifestations among four groups. A: Murine normal liver tissue stained with HE. A1: HE×100, A2: HE×400; B: Demonstration of fatty liver tissues in model control group. Moderate to severe macro vesicular steatosis, diffusely distributed throughout the liver lobule, and parenchymal inflammation with both acute and chronic inflammatory cells accompanying focal necrosis. B1: HE×100, B2: HE×400; C: Significant improvement of liver steatosis in emodin group. There was significant reduction of fatty deposits in liver tissues and the histologic figures restored to nearly normal. C1: HE×100, C2: HE×400; D: Liver steatosis in dietary group. The degree of liver steatosis was improved, but mild steatosis still existed. D1: HE×100, D2: HE×400.