RESUMO
Objective To investigate effects of combined clopidogrel-aspirin treatment for acute cerebral ischemie infarction on a correlation between cerebral microbleeds (CMBs)and hemorrhagic transformation(HT),so as to provide a new evidence for acute phase treatment of ischemic stroke with CMBs.Methods One hundred and forty-eighty patients with acute cerebral infarction meeting the inclusion criteria were consecutively admitted to our hospitals.All patients underwent susceptibility weighted imaging(SWI) to detect CMBs.Patients were classed into two groups:with and without CMBs and subdivided into brain lobe group,deep group and mixed group.The influence of CMBs or not and CMBs different positions on the post-infarction HT was compared.Logistic regression analysis was used to assess the relationship between HT and the related risk factors.Results The 142 patients finally were included in the study,with 64 patients without CMBs and 78 with CMBs.The detection rates of CMBs were 54.9％.Hypertensive prevalence rate(x2 =6.96,P =0.010)and the levels of uric acid (t =2.04,P =0.040) were higher in CMBs group than group without CMBs.The incidence rate of HT was 12.5 ％ (8 cases)in no CMBs group,and 21.8％(17 cases)in the CMBs group(x2 =2.09,P=0.150).6 in 15 patients(40.0％)patients experienced HT in lobar CMBs group;6 patients (12.5 ％)experienced HT in 48 patients with deep CMBs group;5 patients(33.3％)experienced HT in 15 patients with mixed CMBs group.There was statistically significant difference in HT incidence rate(x2 =6.52,P=0.038)among the 3 groups.Lobar CMBs are more vulnerable for HT.Logistic regression analysis showed that atrial fibrillation(OR=6.48,95 ％ CI:2.45-17.19,P =0.000) and hyperglycemia (OR =1.02,95 ％ CI:1.43 1.94,P =0.020) were risk factors for HT,instead of CMBs(OR=1.95,95％CI:0.78-4.87,P=0.150).Conclusions CMBs do not increase the risk of hemorrhage transformation in cerebral ischemic infarction patients at acute stage with combined antithrombotic treatment.While,the double antithrombotic treatment used in patients with the lobar CMBs should be careful.
RESUMO
Objective To investigated the neuroprotective effect of PTEN inhibitor BPV on cerebral ischemia-reperfusion injury in rats and its mechanism. Methods Male Sprague-Dawley rats were used to induce a reperfusion model of middle cerebral artery occlusion for 1 h. During the reperfusion, the BPV solution (0. 2 mg/kg daily) or the equal volume of saline was injected intraperitonealy immediately. The neurological deficit scores were conducted at day 1, 3,5, and 7 after ischemia-reperfusion. At day 4, triphenyl tetrazolium chloride staining was used to assess cerebral infarction volume. Enzyme-linked immunosorbent assay was used to detect the levels of interleukin 10 (IL-10) and tumor necrosis factor α(TNF-α) in cortical ischemic border zones. Real-time quantitative polymerase chain reaction was used to detect the expression level of PTEN mRNA. Western blotting was used to detect the expression levels of PI3K, Akt, and p-GSK-3β. At day 7, Bielschowsky silver staining was used to detect the axonal distribution in the ischemic border zone of the striatum. Immunohistochemical staining was used to detect the expression of myelin basic protein (MBP). Results At day 4 after ischemia-reperfusion, the infarct volume (32. 27% ± 1. 71% vs. 45. 49% ± 2. 12% ; P < 0. 001), TNF-α concentration in the cortical ischemic border zones (134. 17 ± 10. 38 pg/ml vs. 264. 17 ± 24. 84 pg/ml; P < ), and PTEN mRNA level (1. 19 ± 0. 08 vs. 2. 50 ± 0. 06; P < 0. 001) in the rats of the BPV group were al significantly lower than those of the normal saline group. The IL-10 concentration (186. 83 ± 10. 83 pg/ml vs. 147. 83 ± 11. 62 pg/ml; P < 0. 001), and the expression levels of PI3K (0. 43 ± 0. 08 vs. 0. 26 ± 0. 06; P = 0. 004), Akt (0. 52 ± 0. 05 vs. 0. 40 ± 0. 04;P = 0. 001), and p-GSK-3β (0. 75 ± 0. 08 vs. 0. 38 ± 0. 06; P < 0. 001) were al significantly higher than those of the normal saline group. At day 7 after ischemia-reperfusion, the neurological deficit score (4. 83 ± 0. 41 vs. 6. 33 ± 0. 52; P < 0. 001) in the rats of the BPV group was significantly lower than that of the normal saline group. The axon densities in the ischemic border zones (35. 51% ± 2. 45% vs. 25. 31% ± 2. 79% ; P < 0. 001) and the expression level of MBP (32. 56% ± 3. 46% vs. 27. 81% ± 4. 18% ; P = 0. 037) were significantly higher than those of the normal saline group. Conclusions BPV has neuroprotective effect for cerebral ischemia-reperfusion injury in rats. Its mechanism may be associated with the up-regulation of PTEN downstream proteins PI3K, Akt and p-GSK-3β expression to regulate inflammatory mediators and reduce the inflammatory response.