Figure 1.
Chemical structure of danshensu (C9H10O5, molecular weight = 198.17).
Figure 2.
Effect of danshensu on platelet aggregation in normal rats.
Blood was drawn 60 min after intragastric danshensu administration. Platelet aggregation was induced by diphosphate (ADP) and arachidonic acid (AA). Data are expressed as mean ± SEM (each group, n = 10). **P<0.01 with control group.
Figure 3.
Effect of danshensu on platelet aggregation in blood stasis rats.
Blood was drawn 60 min after intragastric danshensu administration. Platelet aggregation was induced by arachidonic acid (AA). Data are expressed as mean ± SEM (each group, n = 10). The blood stasis model was built during the interval between when 2 injections of adrenaline hydrochloride (Adr) were given to rats placed in ice-cold water. ##P<0.01 compared with normal control. *P<0.05 **P<0.01 compared with Adr control.
Figure 4.
Antithrombotic activity of danshensu in the rat model of arteriovenous shunt.
The drug or solvent was administered orally 60 min before thrombogenic challenge. Data are expressed as mean ± SEM (each group, n = 10). Thromb: thrombosis. *P<0.05, **P<0.01, ***P<0.001 compared with thrombotic control group.
Figure 5.
Antithrombotic activity of danshensu in the rat model of ligating inferior vena cava.
The drug or solvent was administered orally 60 min before the thrombogenic challenge. Data are expressed as mean ± SEM (each group, n = 10). Thromb: thrombosis. *P<0.05, **P<0.01, ***P<0.001 compared with thrombotic control group.
Figure 6.
Direct effect of various concentrations of danshensu and aspirin on the enzymatic activities of COX-1 and COX-2.
Danshensu and aspirin (water, as a control) were incubated with COX-1 (A) or COX-2 (B) for 10 min and then AA was added. COX enzyme activities are reflected by the amount of PGE2 produced. PGE2 production was measured by ELISA. Enzyme activity in the sample without treatment (water alone) served as control and results are expressed as inhibitory rate of COX-1 and COX-2 activity compared with solvent control.
Figure 7.
The effects of danshensu on COX expression.
Rats were given 15, 30 and 60 mg/kg danshensu intragastrically and 20 mg/kg aspirin for 7 days. Venous thrombus formation was induced by inferior vena cava (IVC) ligation to produce thrombus after last administration.Vein walls were harvested from venous thrombosis and the expression of COX-1 and COX-2 was assessed by western analysis (A and C). β-actin was measured to confirm equal loading of proteins. Densitometric analysis of COX-1 (B) and COX-2 (D) expression is represented by the mean from 3 separate experiments. Data were normalized to β-actin levels. Thromb: thrombosis. ##P<0.01 compared with normal control. *P<0.05, **P<0.01 compared with thrombotic control group.
Table 1.
Effects of danshensu on plasma TXB2 and 6-keto-PGF1α levels and TXB2-6-keto-PGF1α ratio in rats in the arteriovenous shunt model.
Table 2.
Effects of danshensu on plasma TXB2 and 6-keto-PGF1α levels and TXB2-6-keto-PGF1α ratio in rats the venous thrombosis model.
Table 3.
The effect of danshensu on the hemorheological parameters in rats.
Figure 8.
Gastric ulcerogenic response induced by danshensu and aspirin in rats.
The test compounds were administered orally at the indicated dose (mg/kg) to rats for 7 days. The animals were sacrificed after the last drug administration and the total length of mucosal lesions in each stomach was used to create an ulcer index. Data are presented as the mean ± SEM (each group, n = 10). **P<0.01 versus the control group.
Figure 9.
Effects of danshensu on aspirin-induced gastric lesions in mice.
A: Photographs of gastric mucosa in the control group and danshensu, aspirin and aspirin + danshensu treatment groups are shown. B: The hemorrhagic ulcer index (mm2) for each condition. Values are shown as the mean ± SEM(each group, n = 10). **P<0.01 compared with the control rats. ##P<0.01 compared with the aspirin-treated rats.