Abstract: Objective   To investigate the anti-fibrotic effect of fasudil hydrochloride on Schistosoma japonicum-infected mice， and the effect of fasudil hydrochloride on hepatic stellate cells （HSCs）.   Methods   Thirty female BALB/c mice were randomly divided into 3 groups viz. normal control group （NC group）, infection group, and experiment group. Mice in both infection group and experiment group were infected with （14±2） cercariae of S. japonicum. At 6 weeks post infection, mice in experiment group were intraperitoneally injected with fasudil hydrochloride （10 mg/kg） twice a day for 7 d, while mice in NC group and infection group received the same volume of physiological saline. All mice were sacrificed 12 h after the last injection. Livers from NC group and infection group were used to prepare tissue sections for hematoxylin and eosin （HE） staining, or sirius red staining, and observed under light microscope. Livers from all three groups were used to detect content of hydroxyproline （Hyp） and the mRNA expressions of α-smooth muscle actin （α-SMA）, type Ⅰ collagen α1 （Col1α1） and epithelial cell transforming sequence 2 （Ect2）. HSCs from mice in all three groups were isolated to detect the mRNA levels of α-SMA, Col1α1, and Ect2, respectively.  Results   Pathological sections showed that in livers from mice in infection group, inflammatory cells infiltrated and collagenous fibre proliferated around portal areas and egg granulomas. The content of Hyp in liver from mice of NC group, infection group, and experiment group was （279.7±21.2） μg, （528.0±15.0） μg, and （355.4±22.6） μg, respectively. The content of Hyp in livers from mice of experiment group was significantly reduced compared to infection group （P<0.01）. The mRNA expression of α-SMA, Col1α1 and Ect2 in livers and HSCs from mice in experiment group were significantly down-regulated compared to infection group （P<0.05）.  Conclusion   Fasudil hydrochloride can depress hepatofibrosis in Schistosoma japonicum-infected mice.

Key words: Schistosoma japonicum, Hepatofibrosis, Fasudil hydrochloride, Rho kinase