Background Fibrinogen-depleting agents are promising in the treatment of cerebral ischemic disease. They were studied by many trials, and the outcomes were different because of different regimens and different doses. ...Background Fibrinogen-depleting agents are promising in the treatment of cerebral ischemic disease. They were studied by many trials, and the outcomes were different because of different regimens and different doses. In this study, we assessed the efficacy and safety of defibrase on acute cerebral infarction in China. Methods A search using Chinese hospital knowledge database （CHKD） and MEDLINE database for randomized controlled trials was carded out. A CHKD （1994 June 2005） search was performed with the keyword ＂defibrase＂, then a second search for the keyword ＂acute cerebral infarction＂; a MEDLINE search （1950 June 2005） was performed with the following keywords： [（cerebral ischemia）, OR （acute cerebral infarction）, OR （stroke）], AND [defibrase]. Meta-analysis was performed with RevMan software 4.2. Results Included were 14 studies comparing the efficiency and safety of defibrase with other drugs in the treatment of acute cerebral infarction. Patients＇ records were pooled （total 646 patients; defibrase, n=328, no defibrase n=318）. Neurological deficit score （NDS） before treatment showed weighted mean differences （WMD）=0.95, 95% confidence interval （CI）= （-0.60, 2.50）, P=0.23; NDS after treatment showed WMD=- 2.20, 95% CI= （-4.21, -0.18）, P=0.03; Barthel index at 3 months showed WMD=4.45, 95% CI= （-0.13, 9.03）, P=0.06; the plasma fibrinogen level before treatment showed WMD=0.02, 95% CI= （-0.16, 0.19）, P=0.86; plasma fibrinogen level after treatment showed WMD=- 1.51, 95% CI= （- 1.88, - 1.15）, P〈0.00 001.Conclusions With the given dose and regimen of defibrase in China, defibrase may play a role of anticoagulation. It might inhibit the progression of stroke and prevent the recurrence of stroke.展开更多
Background Atherosclerosis is a complex vascular inflammatory disease. Aspirin is a mainstay in the prevention of vascular complications of atherosclerosis. In this study, the effectiveness of aspirin in suppressing a...Background Atherosclerosis is a complex vascular inflammatory disease. Aspirin is a mainstay in the prevention of vascular complications of atherosclerosis. In this study, the effectiveness of aspirin in suppressing atherosclerosis and the inflammation process was evaluated in rabbits fed with a high fat diet. Methods Eighteen male New Zealand rabbits were randomly divided into 3 groups： control group, untreated cholesterol-fed group, aspirin treated cholesterol-fed group, which were fed for 12 weeks. After 12 weeks, the aorta was harvested for pathologic morphology observation. Immunohistochemical analysis of cyclooxygenase-2 （COX-2）, macrophage and vascular smooth muscle cell （VSMC） was performed. The statistical analysis was performed by the statistical program SPSS 10.0. Results The aorta plaque/intima size （P/I） by pathologic morphology observation was 0%, （59.6± 13.7）% and （36.3±16.5）% in the control, untreated cholesterol-fed group and aspirin treated group, respectively. The maximum plaque thickness, the degree of artery stenosis and the proportion of the intimal circumference occupied by atheroma of the 3 groups were significantly different from each other （P〈0.01）. The expression of COX-2 and macrophage in plaque of the aspirin treated group were decreased compared with that in untreated cholesterol-fed group. However, no difference was found in the expression of VSMC between the aspirin treated and the untreated cholesterol-fed group. Conclusion The mechanism of atherosclerosis suppression by aspirin in cholesterol-fed rabbits is related to the inhibition of COX-2 expression together with the reduced inflammation followed by, but not related to the hypolipidemic effects.展开更多
Background This study investigated the inhibitory effect of berberine （BBR） on lipopolysaccharide （LPS） induced cyclooxygenase-2 （COX-2） expression via the mitogen activated protein kinase （MAPK） signalling ca...Background This study investigated the inhibitory effect of berberine （BBR） on lipopolysaccharide （LPS） induced cyclooxygenase-2 （COX-2） expression via the mitogen activated protein kinase （MAPK） signalling cascade pathways in human peripheral blood monocytes （PBMC）. Methods PBMC from whole blood were isolated and cultured for up to 24 hours after division into 5 groups treated with LPS, LPS＋BBR 25 μmol/L, LPS＋BBR 50 μmol/L or LPS＋BBR 100 μmol/L and untreated. Monocytes were extracted for RT-PCR and Western blot analyses to examine COX-2 mRNA and protein activated expression of p38 mitogen activated protein kinase （p38MAPK）, Jun N-terminal kinase （JNK） and extracellular regulated kinases 1/2 （ERK1/2） signalling pathways. Results COX-2 mRNA and protein expression decreased to a minimum at 12 hours after BBR treatment （P 〈0.05）. With the increasing concentration of BBR treatment, the COX-2 expression decreased progressively （P 〈0.01）. With BBR treatment for 6, 12 or 24 hours at three doses, ERK1/2 protein expression was significantly inhibited. For the JNK pathway, only with the treatment of BBR at the concentration of 100 μmol/L was JNK protein expression inhibited compared with the LPS stimulation group （P 〈0.01）. Irrespective of the BBR concentration, no difference was shown between the BBR group and the LPS group for p38MAPK protein expression. Human monocytes COX-2 mRNA, by RT-PCR, and protein expression, by Western blot analysis, were inhibited when incubated with PD98059, SP600125 and SB203580 （P 〈0.05）. Conclusions Berberine inhibits COX-2 expression via the ERK1/2 signalling pathway and, possibly, at a high dosage via the JNK pathway. P38MAPK may have no relationship with the effect of BBR in PBMC. Berberine inhibited COX-2 mRNA and protein expression in a dose dependent manner and suppressed COX-2 expression to a minimal level after 12 hours of berberine treatment.展开更多
文摘Background Fibrinogen-depleting agents are promising in the treatment of cerebral ischemic disease. They were studied by many trials, and the outcomes were different because of different regimens and different doses. In this study, we assessed the efficacy and safety of defibrase on acute cerebral infarction in China. Methods A search using Chinese hospital knowledge database （CHKD） and MEDLINE database for randomized controlled trials was carded out. A CHKD （1994 June 2005） search was performed with the keyword ＂defibrase＂, then a second search for the keyword ＂acute cerebral infarction＂; a MEDLINE search （1950 June 2005） was performed with the following keywords： [（cerebral ischemia）, OR （acute cerebral infarction）, OR （stroke）], AND [defibrase]. Meta-analysis was performed with RevMan software 4.2. Results Included were 14 studies comparing the efficiency and safety of defibrase with other drugs in the treatment of acute cerebral infarction. Patients＇ records were pooled （total 646 patients; defibrase, n=328, no defibrase n=318）. Neurological deficit score （NDS） before treatment showed weighted mean differences （WMD）=0.95, 95% confidence interval （CI）= （-0.60, 2.50）, P=0.23; NDS after treatment showed WMD=- 2.20, 95% CI= （-4.21, -0.18）, P=0.03; Barthel index at 3 months showed WMD=4.45, 95% CI= （-0.13, 9.03）, P=0.06; the plasma fibrinogen level before treatment showed WMD=0.02, 95% CI= （-0.16, 0.19）, P=0.86; plasma fibrinogen level after treatment showed WMD=- 1.51, 95% CI= （- 1.88, - 1.15）, P〈0.00 001.Conclusions With the given dose and regimen of defibrase in China, defibrase may play a role of anticoagulation. It might inhibit the progression of stroke and prevent the recurrence of stroke.
文摘Background Atherosclerosis is a complex vascular inflammatory disease. Aspirin is a mainstay in the prevention of vascular complications of atherosclerosis. In this study, the effectiveness of aspirin in suppressing atherosclerosis and the inflammation process was evaluated in rabbits fed with a high fat diet. Methods Eighteen male New Zealand rabbits were randomly divided into 3 groups： control group, untreated cholesterol-fed group, aspirin treated cholesterol-fed group, which were fed for 12 weeks. After 12 weeks, the aorta was harvested for pathologic morphology observation. Immunohistochemical analysis of cyclooxygenase-2 （COX-2）, macrophage and vascular smooth muscle cell （VSMC） was performed. The statistical analysis was performed by the statistical program SPSS 10.0. Results The aorta plaque/intima size （P/I） by pathologic morphology observation was 0%, （59.6± 13.7）% and （36.3±16.5）% in the control, untreated cholesterol-fed group and aspirin treated group, respectively. The maximum plaque thickness, the degree of artery stenosis and the proportion of the intimal circumference occupied by atheroma of the 3 groups were significantly different from each other （P〈0.01）. The expression of COX-2 and macrophage in plaque of the aspirin treated group were decreased compared with that in untreated cholesterol-fed group. However, no difference was found in the expression of VSMC between the aspirin treated and the untreated cholesterol-fed group. Conclusion The mechanism of atherosclerosis suppression by aspirin in cholesterol-fed rabbits is related to the inhibition of COX-2 expression together with the reduced inflammation followed by, but not related to the hypolipidemic effects.
文摘Background This study investigated the inhibitory effect of berberine （BBR） on lipopolysaccharide （LPS） induced cyclooxygenase-2 （COX-2） expression via the mitogen activated protein kinase （MAPK） signalling cascade pathways in human peripheral blood monocytes （PBMC）. Methods PBMC from whole blood were isolated and cultured for up to 24 hours after division into 5 groups treated with LPS, LPS＋BBR 25 μmol/L, LPS＋BBR 50 μmol/L or LPS＋BBR 100 μmol/L and untreated. Monocytes were extracted for RT-PCR and Western blot analyses to examine COX-2 mRNA and protein activated expression of p38 mitogen activated protein kinase （p38MAPK）, Jun N-terminal kinase （JNK） and extracellular regulated kinases 1/2 （ERK1/2） signalling pathways. Results COX-2 mRNA and protein expression decreased to a minimum at 12 hours after BBR treatment （P 〈0.05）. With the increasing concentration of BBR treatment, the COX-2 expression decreased progressively （P 〈0.01）. With BBR treatment for 6, 12 or 24 hours at three doses, ERK1/2 protein expression was significantly inhibited. For the JNK pathway, only with the treatment of BBR at the concentration of 100 μmol/L was JNK protein expression inhibited compared with the LPS stimulation group （P 〈0.01）. Irrespective of the BBR concentration, no difference was shown between the BBR group and the LPS group for p38MAPK protein expression. Human monocytes COX-2 mRNA, by RT-PCR, and protein expression, by Western blot analysis, were inhibited when incubated with PD98059, SP600125 and SB203580 （P 〈0.05）. Conclusions Berberine inhibits COX-2 expression via the ERK1/2 signalling pathway and, possibly, at a high dosage via the JNK pathway. P38MAPK may have no relationship with the effect of BBR in PBMC. Berberine inhibited COX-2 mRNA and protein expression in a dose dependent manner and suppressed COX-2 expression to a minimal level after 12 hours of berberine treatment.
