Meta-analysis of defibrase in treatment of acute cerebral infarction / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>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.</p><p><b>METHODS</b>A search using Chinese hospital knowledge database (CHKD) and MEDLINE database for randomized controlled trials was carried 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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>

Effects of aspirin on atherosclerosis and the cyclooxygenase-2 expression in atherosclerotic rabbits / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>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.</p><p><b>METHODS</b>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 SPSS10.0.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

The expression of matrix metalloproteinases-9, transforming growth factor-beta1 and transforming growth factor-beta receptor I in human atherosclerotic plaque and their relationship with plaque stability / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Transforming growth factor-beta (TGF-beta) and matrix metalloproteinases-9 (MMP-9) have been implicated in the pathogenesis of human atherosclerosis but their relationship during lesion progression are poorly understood. The objective of this study was to investigate the expression of MMP-9, TGF-beta1 and TGF-beta receptor I (TbetaR-I) in human atherosclerotic plaque and their relationship and plaque stability.</p><p><b>METHODS</b>Specimens of human coronary artery atherosclerotic plaques were obtained from 41 patients undergoing coronary endarterectomy, and were paraffin embedded, sectioned at 4 microm intervals then stained with haematoxylin and eosin. They were divided into stable (with no or only little lipid core) and unstable plaque groups (with lipid core size > 40%): the immunohistochemical staining were performed for MMP-9, TGF-beta1 and TbetaR-I.</p><p><b>RESULTS</b>The expression of MMP-9 in the unstable plaques was much higher than in the stable ones, but the expression of TGF-beta1 was higher in the stable plaques. There was no similar significant difference for TbetaR-I. Correlation analysis showed that there was a negative correlation between the expression of MMP-9 and TGF-beta1 (r = -0.332, P = 0.034 for average areal density; r = -0.373, P = 0.016 for average optical density).</p><p><b>CONCLUSIONS</b>There were close relationships between MMP-9, TGF-beta1 and plaque stability. Enhanced production of MMP-9 may participate in the formation of unstable plaque, while TGF-beta1 maybe an important stabilizing factor in preventing transition into an unstable plaque phenotype.</p>