OBJECTIVE: To investigate the preventive effects of a compound Danshen preparation (DSC) on long-term gastric lipid emulsion administration-induced nonalcoholic steatohepatitis in rats. METHODS: Twenty-seven 3-month-old SD rats were randomized equally into 3 groups and subjected to daily intragastric administration for 20 weeks of distilled water (control), lipid emulsion at 5 ml/kg (model group), and lipid emulsion plus DSC at 5.0 g/kg (DSC treatment group). After blood glucose (BG) determination, the rats were sacrificed for measurement of serum TC, TG, HDL-c, AST, and ALT, and the liver was weighed and pathologically examined. RESULTS: Compared with the control group, the rats in the model group showed significantly increased BG, TC, LDL-c, arteriosclerosis index (AI), AST, ALT, liver weight, and liver index (P<0.01) and decreased HDL-c (P<0.01), while TG remained unchanged. Fatty degeneration, hydropic degeneration and necrosis with inflammatory cell infiltration were observed in the liver of the rats in the model group. Compared with the model group, the rats in DSC groups showed decreased BG, AI (P<0.01), liver weight, liver index, AST, and ALT (P<0.05) and increased HDL-c, with milder pathological changes in the liver. CONCLUSIONS: Long-term gastric perfusion of lipid emulsion causes lipid metabolic disorder and nonalcoholic fatty liver disease in rats characterized by increased TC and decreased HDL-c. DSC can significantly increase HDL-c and provide partial protection of the liver against the damages by the lipid emulsion.
OBJECTIVE: To investigate the preventive effects of a compound Danshen preparation (DSC) on long-term gastric lipid emulsion administration-induced nonalcoholic steatohepatitis in rats. METHODS: Twenty-seven 3-month-old SD rats were randomized equally into 3 groups and subjected to daily intragastric administration for 20 weeks of distilled water (control), lipid emulsion at 5 ml/kg (model group), and lipid emulsion plus DSC at 5.0 g/kg (DSC treatment group). After blood glucose (BG) determination, the rats were sacrificed for measurement of serum TC, TG, HDL-c, AST, and ALT, and the liver was weighed and pathologically examined. RESULTS: Compared with the control group, the rats in the model group showed significantly increased BG, TC, LDL-c, arteriosclerosis index (AI), AST, ALT, liver weight, and liver index (P<0.01) and decreased HDL-c (P<0.01), while TG remained unchanged. Fatty degeneration, hydropic degeneration and necrosis with inflammatory cell infiltration were observed in the liver of the rats in the model group. Compared with the model group, the rats in DSC groups showed decreased BG, AI (P<0.01), liver weight, liver index, AST, and ALT (P<0.05) and increased HDL-c, with milder pathological changes in the liver. CONCLUSIONS: Long-term gastric perfusion of lipid emulsion causes lipid metabolic disorder and nonalcoholic fatty liver disease in rats characterized by increased TC and decreased HDL-c. DSC can significantly increase HDL-c and provide partial protection of the liver against the damages by the lipid emulsion.