Objective     To determine the effect of the targeting expression of rat interleukin-10 (rIL-10) gene in the liver on the progress of porcine serum-induced hepatic fibrosis in rats.     Methods     pcDNA3-rIL-10 was transferred to the rat liver by hydrodynamic-based transfection. RT-PCR and SP-immunohistochemistry analysis were used to detect the expression and distribution of rIL-10 mRNA and protein in the kidneys

lungs

spleen

liver and heart in 24 h after transfection. A total of 30 clean-grade male SD rats were randomly divided into normal control group (n=6)

liver fibrotic model group (n=8)

rIL-10 treatment group (n=8) and null-plasmid control group (n=8). Rat liver fibrotic model was established by intraperitoneal injection of pig serum

0.5 ml/d

twice a week for 8 weeks

and the rats of normal control group received an injection of saline. From the 5th week after pig serum injection

the rats of the later 3 groups underwent an intraperitoneal injection of Ringer’s solution containing 1 μg/g pcDNA3-rIL-10 or pcDNA3 through tail vein once a week. At the end of the 8th week

all rats were put to death and then collected blood and liver sample. HE staining was used to detect the changes of liver tissue sections pathomorpholohy. The change of ALT and AST in serum and collagen type Ⅰ

Ⅲ in the liver were measured by biochemistry analysis and Picrosirius staining respectively.     Results     RT-PCR and immunohistochemistry confirmed that the presence of rIL-10 transcription and expression mainly in the liver. HE staining showed that rat hepatic fibrosis model induced by pig serum was established successfully. Compared with the null-plasmid control group

the liver in the fibrotic model group showed hepatocytic fatty degeneration

inflammatory cells invasion

massive collagen deposition to form fiber partition in difference thickness

and even false hepatic lobules. Compared with liver fibrotic model and null-plasmid control group

rIL-10 treatment group showed significant therapeutic effects: decreased necrosis in hepatocytes and lesser invasive inflammatory cells

reduced the disposition of collagen fibers and the lower levels of ALT and AST in the serum (P0.01)

significantly inhibited expression of collagen type Ⅰ and Ⅲ (P0.01).     Conclusion     Injection of pcDNA3-rIL-10 via tail vein in rats results in targeting expression of rIL-10 in the liver

and efficiently prevent the progression of hepatic fibrosis induced by pig serum.