RESUMO
Objective To investigate the protective role of Xiongbitong capsule against liver injury in hyperlipemic rats.Methods Sixty Wistar male rats were randomly divided into 5 groups(12 rats in each group): a blank group, a model group, a simvastatin group(10 mg/kg, 2 ml intragastric administration daily), a Xiongbitong capsule high-dose group(25 mg/kg, 2 ml intragastric administration daily), and a Xiongbitong capsule low-dose group(12.5 mg/kg, 2 ml intragastric administration daily). Hyperlipidemia model in rats was indeuced by hyperlipidemic diet. The simvastatin group was intragastric administrated with simvastatin suspension 2 ml(10 mg/kg daily), and the rats in the control group and the model group were intragastric administrated with equal volume of saline. After 10 weeks, the serum leves of total cholesterol(TC), triacylglycerol(TG), low-density lipoprotein cholesterol(LDL-C), high-density lipoprotein cholesterol (HDL-C), nitric oxide(NO), endothelin1(ET-1), and the whole blood viscosities(high-, medium-, low-shear)were measured. Liver injury were evaluated with histopathologic examination by H.E. staining. The expressions of intercellular adhesion molecule-1(ICAM-1), monocyte chemoattractant protein-1(MCP-1)in hepatic tissue were measured by immunohistochemical staining.Results The serum leves of TC(1.47± 0.10 mmol/Lvs. 3.48±0.19 mmol/L), TG(0.38±0.11 mmol/Lvs. 0.95±0.14 mmol/L), LDL-C(1.48± 0.18 mmol/Lvs. 2.39±0.22 mmol/L), ET-1(145.81±18.65 pg/mlvs. 177.70±17.70 pg/ml) in the Xiongbitong capsule high-dose group were significantly lower than those in the model group(allP<0.01), HDL-C(1.21±0.14 mmol/Lvs. 0.65±0.10 mmol/L)and NO(31.28±2.36μmol/Lvs. 19.61±1.28μmol/L) significantly lower than those in the model group(allP<0.01), the expressions of ICAM-1(0.133±0.019vs. 0.187±0.011)and MCP-1(0.153±0.014vs. 0.264±0.020)significantly lower than those in the model group(allP<0.01). The liver injury in the Xiongbitong capsule high-dose group decreased than that in the model group. Conclusions Xiongbitong capsule can protect against liver injury via regulating lipid metabolism, protecting endothelial function and down regulating expressions of MCP-1 and ICAM-1.
