Objective To investigate the effect of intravenous thrombolytic therapy with urokinase on the neurological function and the concentration of serum matrix metalloproteinase 9 (MMP-9) in the patients with acute cerebral infarction.Methods The patients with acute cerebral infarction were divided into the experimental and control groups.The experimental group included 27 patients who were complied with thrombolytic criterion within 4.5 hours after stroke and were firstly treated by intravenous thrombolytic therapy with urokinase by 100 million units after 24 h and 300 mg aspirin by oral.The control group included 27 cases that were directly administrated by 300 mg aspirin 4.5 hours later after stroke.After 24 h,the two groups were administrated with other same conventional treatments such as neurotrophy,improvement of microcirculation,and control of blood-fat.The neurological function and dynamic concentration of serum MMP-9 were observed before treatment and after treatment.Results After treatment,the neurological deficit evaluation score in both groups was gradually reduced with the treatment time,and the neurological deficit evaluation score in the experimental group was significantly lower than that in the control group at the 1 st,3rd,and 14th day,respectively[(10.97 ± 1.53) Score vs (15.67 ±1.78)Score,t =8.35,P =0.03;(8.15 ± 1.40) Score vs(12.72 ± 3.31) Score,t =6.62,P =0.03; (5.87 ± 1.03) Score vs (11.92 ±2.05) Score,t =13.70,P =0.01].After treatment,the concentration of serum MMP-9 in both groups was reduced with the treatment time,and serum MMP-9 in the experimental group was significantly lower than that in the control group at the 1st,3rd,and 14th day,respectively[(282.84 ±37.51) ng/ml vs (316.90±36.75)ng/ml,t =3.37,P =0.00;(309.11±37.71)ng/mlvs (348.39 ±15.26) ng/ml,t =5.02,P=0.04;(264.68±31.91)ng/ml vs (302.81 ±36.30)ng/ml,t =4.10,P =0.03].Conclusions Intravenous thrombolytic therapy with urokinase can effectively reduce the neurological deficit and the produce of MMP-9 in patients with acute cerebral infarction.

Objective To investigate the effects on proliferation of multiple myeloma cell lines U266 and RPMI 8226 induced by puerariae radix flavones (PRF) in vitro and its possible mechanism.Methods Exposed to 0,10,30,50,100 μg/ml PRF for 48 h and 72 h,the U266 and RPMI 8226 cells proliferation inhibitory rates were detected by MTT assay,cell cycles by flow cytometry (FCM),morphologic changes of U266 cells by Wright' s staining,and early-stage apoptotic rates of U266 cells by FITC-Annexin V/PI staining with FCM.Analysis of DNA fragment was made to test characteristic apoptosis DNA ladder in U266 cells.Results 0,10,30,50,100 μg/ml PRF could inhibit the proliferation of U266 and RPMI 8226 cells in a dose-dependent manner (U266 ＞ RPMI 8226).Cell cycle analyses in U266 and RPMI 8226 cells showed that sub-diploid peaks,but cell cycles changed minor.Wright's staining of U266 cells showed hardly any apoptostic character istic.Annexin V/PI double staining indicated that early-stage apoptotic rates of U266 cells exposed to 0,10,30,50,100 μg/ml PRF for 48 h were mildly increased in a dose-dependent manner.They were (3.20±0.36) ％,(5.20±0.92) ％,(7.30±1.22) ％,(8.10±0.53) ％ and (10.80±0.90) ％,respectively.The group differences had statistical significance (P ＜ 0.05).Analysis of DNA fragment barely exhibited the characteristic DNA ladder in U266 cells.Conclusion A certain concentrations of PRF could inhibit the proliferation of U266 and RPMI 8226 cells significantly.It is suggested that apoptosis related to the proliferative inhibition mechanism induced by PRF in U266 cell line,but not main.Other pathways such as necrosis and autophagy whether or not involved need further investigation.