| Salvianolate, which is extracted from Salvia miltiorrhiza and mainly composed of polyphenolic compound magnesium lithospermate B and its analogues, is the most important composition in Salviae miltiorrhizae and exerts beneficial effects in cardiovascular disease. In the present paper, we aimed to investigate the effects of Salvianolate on lipid peroxidation, LDL oxidation induced by Cu2+ or human macrovascular endothelial cell (HMEC), platelet aggregation of rat plasma induced by ADP, and the potential treatment of atherosclerosis rabbits.Salvianolate 3, 30 mg/L significantly inhibited lipid peroxidation of rat tissue homogenate (P<0.01). In the liver, kidney, heart and brain homogenate, the inhibitory rate of Salvianolate 30 mg/ml was 61.3%, 57.7%, 55.1%, and 54.0%, respectively. The effect of Salvianolate on the TBARS formation of LDL induced by Cu2+ was detected using the fluorimetric method. The results indicated that Salvianolate 0.3, 1.0, 3.0 mg/L significantly inhibited the TBARS formation (P<0.01), and the inhibitory rate was 8.14%, 70.19%, 97.35%, respectively. The effect of Salvianolate on the relative electrophoretic mobility (REM) of LDL induced by Cu2+ was studied by agarose gel electrophorosis. The results showed that in the presence of Salvianolate 0.3, 1.0, 3.0 mg/L, REM induced by oxidation decreased (P<0.01). The TBARS formation and the REM induced by HMEC were also decreased significantly (P<0.01). These results indicate that Salvianolate concentration -dependently inhibits the oxidative modification of LDL. The effects of Salvianolate on platelet aggregation were measured by means of turbidimetry in platelet-rich plasma of rats. Salvianolate 0.5, 0.8, 1.0 mg/ml can significantly inhibited the platelet aggregation induced by ADP (P<0.01), and the inhibitory rates were 25.1%, 7.1%, 49.5%, respectively. Salvianolate 0.5, 0.8, 1.0 mg/ml also can reduce Tm. These results indicate that Salvianolate concentration-dependently inhibits the aggregation induced by ADP in rat platelets.The antiatherogenic effect of Salvianolate was investigated in cholesterol-fed rabbits, which were divided four groups one for atherogenic control, one for administration with 50 mg/kg pravastatin sodium, and the other two groups each for administration with 10 or 50 mg/kg Salvianolate. New Zealand white male rabbits were fed diets containing 0.5 g/100 g cholesterol to induce the formation of atherosclerosis for 10 weeks, and also administrated Savianolate or Pravastatin sodium simultaneously. We observed the effects of Savianolate on the content of serum lipid, vascular endothelial function, and TBARS concentration in heart, brain, kidney, vessel and serum of rabbits at the end of 10 weeks. Content of T-CHO and LDL-C in Salvianolate administrated groups are slightly lower than in atherogenic control group (P>0.05). Formation of TBARS in the homogenates of heart, liver and kidney in these two groups has a significant decrease compared with the atherogenic control group (P<0.05), but not in vessel and serum (P>0.05). Content of cholesterol in the liver homogenate and vascular endothelial function between Salvianolate administrated groups and atherogenic control group have no significant difference (P>0.05). The extent of atherosclerosis in the thoracic aorta was significantly reduced in the Salvianolate 50 mg/kg group, compared with atherogenic control group (P<0.05). However, atherosclerotic lesion area in the aortic arch and total atherosclerotic plaque were not affected in Salvianolate administrated groups. Histopathological analysis showed Salvianolate could alleviate the pathological alterations in atherosclerotic plaques of the thoracic aorta. Compared with atherogenic control group, fewer extracellular lipid deposits and macrophage-derived foam cells were observed in the intimal lesions of the thoracic aorta in Salvianolate administrated groups. In conclusion, Salvianolate inhibited the lipid peroxidation, the oxidative modification of LDL, and the aggregation of rat platelets, in add...
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