Abstract: Objective To investigate the protective effect of astaxanthin on hepatic fibrosis and the mechanism by which the TGF-β1/Smad/ERK pathway involved. Methods 50 male SD rats were randomly divided into control,model,colchicine （0.1 mg·kg^-1）,astaxanthin group I （2 mg·kg^-1） and astaxanthin groupⅡ（4 mg·kg^-1）-intervened groups with 10 rats in each group. A rat model of hepatic fibrosis was established by subcutaneous injection of carbon tetrachloride. At 10th week of modeling,rats in each group were respectively given intragastric administration of colchicines or astaxanthin except in control and model with normal salt,for 6 weeks. The expression of type I collagen,Smad2,transforming growth factor-β1（TGF-β1） and p-ERK protein in liver tissues was detected by immunohistochemistry and Western blot,and the collagen I,Smad2,TGF- beta 1 and p-ERK mRNA in liver tissues was detected by RT-PCR. Results The collagen I protein in the liver tissues of control,astaxanthin group I and astaxanthin group II were （0.4±0.1）,（1.4±0.3） and （1.2±0.3）,respectively,significantly lower than [（1.7±0.4）,P<0.05] in the model,Smad2 protein was（0.5±0.1）,（1.3±0.4） and（0.8±0.4）,much lower than [（1.6±0.3）,P<0.05] in the model,TGF-β1 protein was（0.5±0.1）,（1.4±0.4） and （1.4±0.4）,significantly lower than[（1.7±0.4）,P<0.05] in the model,and the p-ERK protein was（0.4 ± 0.1）,（1.3±0.4） and（0.9±0.3）,respectively,also significantly lower than[（1.6±0.5）,P<0.05] in the model;the hepatic collagen I mRNA levels in the control,astaxanthin group I and astaxanthin group II were （1.0±0.1）,（2.0±0.4） and （1.8±0.5）,significantly lower than[（2.4±0.4）,P<0.05] in the model,the Smad2 mRNA were（1.0 ± 0.1）,（2.0±0.5） and （1.8±0.4）,significantly lower than[（2.5±0.6）,P<0.05] in the model,the TGF-β1 mRNA were（1.0±0.1）,（2.1±0.4） and （1.6±0.3）,much lower than [（2.5±0.5）,P<0.05] in the model,and the p-ERK mRNA levels were （1.1±0.1）,（2.1±0.4） and（1.8±0.3）,respectively,also significantly lower than[（2.6±0.5）,P<0.05] in the model. Conclusion Astaxanthin can inhibit the progression of hepatic fibrosis,which might be related to the down-regulation of TGF-β1/Smad/ERK pathway activation.

Key words: Hepatic fibrosis, Astaxanthin, TGF-β1/Smad/ERK pathway, Rats