ABSTRACT
Objective To investigate the correlation between plasma cystatin C (CysC) level and carotid atherosclerotic plaque in patients with ischemic stroke.Methods The clinical data in patients with acute ischemic stroke were analyzed retrospectively.According to the results of carotid artery ultrasound,the patients were divided into either a non-plaque group or a plaque group.Then the plaque group was redivided into a stable plaque subgroup and a vulnerable plaque subgroup.Multivariate logistic regression analysis and Pearson correlation analysis were used to explore the risk factors for carotid atherosclerotic plaque.Results A total of 226 patients with acute ischemic stroke were enrolled,172 of them had carotid plaque,and 54 had no plaque.Of the patients with carotid plaque,94 were stable plaque and 78 were vulnerable plaque.The age (71.82 ± 9.94 years vs.60.74 ± 13.81 years; t =6.160,P =0.014),proportion of patients with ischemic heart disease (11.6％ vs.1.9％; x2=6.169,P=0.020),systolic blood pressure (148.770± 21.007 mm Hg vs.142.240 ± 19.404 mm Hg; t =2.029,t =0.044),plasma CysC concentration (1.046 ± 0.438 mg/L vs.0.860 ±0.214 mg/L; t =3.006,P =0.003),and carotid IMT (1.122 ±0.278 mm vs.0.878 ±0.250 mm; t =5.762,P=0.000) in the plaque group were significantly higher than those in the non-plaque group.Multivariate logistic regression analysis showed that the age (odds ratio [OR] 1.079,95％ confidence interval [CI] 1.044-1.116; P=0.000) and IMT (OR 31.450,95％ CI 6.233-158.692; P=0.000) was the independent risk factor for carotid plaque,while there was no significant independent correlation between the plasma CysC level and carotid plaque (P =0.217).Only IMT in the stable plaque subgroup was significantly higher than the vulnerable plaque group (1.176 ±0.285 mm vs.1.058 ±0.258 mm; t =-2.824,P =0.005),and it was the independent protective factor for the carotid plaque stability (OR 0.195,95％ CI 0.059-0.064; P =0.007).Pearson correlation analysis showed that the plasma CysC level was positively correlated with the age (r =0.375,P =0.000) and serum creatinine level (r =0.462,P =0.000),but it was not significantly correlated with carotid IMT (r =0.075,P =0.264).Conclusions In patients with ischemic stroke,no correlations were found between the plasma CysC level and carotid atherosclerotic plaque,plaque stability,and IMT.
ABSTRACT
Objective To investigate the effect of tumor necrosis factor receptor 1 (TNFR1) in angiogenesis and neurogenesis during cerebral ischemia in mice.Methods Twenty-four wild-type and 24 TNFR1 knockout mice were randomly divided into either a sham operation group or a focal cerebral ischemia group (n =12 in each group).5-bromodeoxyuridine (BrdU) was injected intraperitoneally at day 3 after cerebral ischemia and sham operation.At day 7 and 28 after cerebral ischemia,the double-label immunofluorescence staining of glucose transporter-1(Glut-1)/BrdU was used to evaluate the angiogenesis surrounding the areas of infarction.A labeled BrdU was used to detect the neural stem cell proliferation in the subventricular zone.Double-labeled doublecortin (DCX)/BrdU and neuronal nuclei antigen (NeuN)/BrdU were used to detect the migration and survival of neural stem cells,respectively.Results Under the normal condition,there was no significant difference in angiogenesis and the number of BrdU-positive cells in the subependymal zone (SVZ) between the wild-type (418.000 ± 28.404) and TNFR1 knockout (528.000 ± 60.597) mice (t =-1.644,P =0.131).At day 7 after cerebral ischemia,the number of Glut-1/BrdU-positive cells in the TNFR1 knockout mice was significantly less than that in the wild-type mice (14.833 ± 2.182 vs.27.5 ± 4.209) (t =2.672,P =0.023),and the number of DCX/B3rdU-positive cells was also significantly less than that in the wild-type mice (163.000 ± 11.106 vs.257.168 ± 12.213) (t =5.705,P =0.000).At day 28 after cerebral ischemia,the number of NeuN/BrdU-positive cells in the TNFR1 knockout mice was significantly less than that in the wildtype mice (6.000 ± 0.577 vs.11.000± 1.571) (t=2.988,P=0.014).Conclusions TNFR1 may play a promoting role in the neurovascular reggeneration in late cerebral ischemia.