[Model establishment of liver fibrosis in oral arsenic solution exposed mice].

OBJECTIVE: To discuss and compare the model establishment of liver fibrosis in oral arsenic solution exposed mice and mice with high-fat feedstuff. METHODS: A total of 240 mice were divided randomly into 6 groups: control group, sodium arsenite group, sodium arsenate group, high-fat feedstuff group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff with 40 mice each. Control group and high-fat feedstuff group (drinking tap water), sodium arsenite group and sodium arsenite group with high-fat feedstuff (drinking 300 mg/L iAs3+ water), sodium arsenate group and sodium arsenate group with high-fat feedstuff (drinking 300 mg/L iAs5+ water). The mice were sacrificed after 3, 6, 10 months' arsenic-exposure and examined for liver function. HE dyeing and Masson dyeing were also employed to observe the pathological changes in hepatic tissue in each group. RESULTS: After 3 months' modeling, ALT and AST in control group, sodium arsenite group, sodium arsenate group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff were (36.7 +/- 5.7) U/L and (110 +/- 22) U/L, (55.6 +/- 4.6) U/L and (249 +/- 41) U/L, (52.6 +/- 8.8) U/L and (161 +/- 15) U/L, (311.3 +/- 19.7) U/L and (484 +/- 15) U/L and (515.0 +/- 60.8) U/L and (671 +/- 24) U/L. They were higher in all the arsenic groups than in control group (P < 0.05); all the HE dyeing samples in arsenic groups showed liver injury in varying degrees such as hydropic degeneration, fatty degeneration, spotty necrosis, focal necrosis and inflammatory cell infiltration. There were liver cell regeneration and fibroplasia in varying degrees. The liver injury of the mice in all arsenic groups aggravated as exposure time prolonged. Masson dyeing after 10 months' modeling showed hyperplasia in portal areas and central venous areas; the mean area of fibrosis in control group, sodium arsenite group, sodium arsenate group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff were 0.1333, 0.5584, 0.5250, 0.7534 and 0.7200 respectively. There was statistical significance between arsenic groups and control group (P < 0.05) CONCLUSION: The liver injury and fibrosis model in oral arsenic solution exposed mice and those with high-fat feedstuff are successfully established and subsequently evaluated. It is a comparatively ideal animal model for studying arsenic liver injury and fibrosis.