[Effect of depsides salts from salvia miltiorrhiza on functions of platelet and vascular endothelial cell of patients with chronic obstructive pulmonary disease in acute exacerbation stage].

OBJECTIVE: To investigate the influence of depsides salts from salvia miltiorrhiza (DSM) on the functions of platelet and vascular endothelial cell in severe chronic obstructive pulmonary diseases (COPD) patients with acute exacerbation. METHODS: Forty patients with severe COPD in acute exacerbation stage were randomly divided into two groups: conventional treatment (CT) group and DSM treatment (DSM) group, each consisting of 20 cases, and 20 healthy adults served as control group. All COPD patients were given conventional treatment, while for the patients in DSM group 0.2 g depsides DSM was given through intravenous drip everyday in addition for 2 weeks. The levels of the plasma platelet membrane glycoprotein 140 (GMP140) and von Willebrand factor (vMF) in the blood samples were determined with enzyme linked immunosorbent assay (ELISA) and the level of CD62P/CD61 with flow cytometry (FCM). RESULTS: The level of GMP140 [CT group: (17.51+/-2.75) microg/L, DSM group: (16.94+/-2.57) microg/L], vMF [CT group: (13.64+/-2.37) microg/L, DSM group: (14.14+/-2.17) microg/L] and CD62P/CD61 [CT group: (20.24+/-2.64)% , DSM group: (19.54+/-2.69)%] were elevated significantly in severe COPD patients with acute exacerbation compared to the control group before treatment [(11.21+/-1.11)%, (9.25+/-1.80) microg/L, (6.13+/-1.17) microg/L, all P<0.01]. After intervention, the levels of the above three indexes in both treatment groups were significantly decreased, and the decrease in DSM group [GMP140: (3.91+/- 0.57) microg/L , vWF: (3.86+/-0.71) microg/L, CD62P/CD61: (3.69+/-0.62)%] was more prominent than the CT group [GMP140: (2.30+/-0.33) microg/L, vWF: (2.72+/- 0.45) microg/L , CD62P/CD61: (2.24+/-0.45)%, all P<0.01], but they were higher than normal levels. CONCLUSION: DSM has the effect of inhibiting the activation of vascular endothelial cells and platelet. The medicine may be used to prevent thrombotic diseases.

[Effect of ulinastain on the expression of hemeoxygenase-1 in oleic acid-induced acute lung injury in rats].

OBJECTIVE: To explore the effect of ulinastain on the expression of hemeoxy genase-1 (HO-1) in oil acid-induced acute lung injury in rats. METHODS: The animal model of acute lung injury was established by oil acid. Thirty SD rats were randomly divided into 3 groups: the blank control group (A), the acute lung injury group (B) and the acute lung injury group (C) followed by injecting 100 mL/kg ulinastatin. Each group consisted of 10 rats. Group A were given 0.2 mL/kg natural solution through the trial vein; Group B and C were given 0.2 mL/kg oil-acid through trial vein, while group C were injected 100mL/kg ulinastatin by the peritoneal cavity after injecting oil acid. After 4 hours, the rates of respiration were counted and blood samples were cramped out through the heart puncture for blood gas analysis. The expressions of hemeoxygenase-1 and the pathologic construction changes were determined by HE staining in the lower right lung of rats in the 3 groups. RESULTS: The respiration dysfunction caused by oil acid could be prominently improved by ulinastain. There was only a little expression of hemeoxygenase-1 in the lung of Group A, but the expression increased in Group B and significatively increased in Group C. CONCLUSION: Ulinastatin may protect the rats from acute lung injury through increasing the expression of HO-1.