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ObjectiveToinvestigatethecorrelationbetweenbloodpressurevariabilityandcognitive impairment in ischemic stroke. Methods The inpatients with acute ischemic stroke were enroled. The demographic and clinical data were colected. The coefficient of variation of blood pressure within 7 days after onset w as calculated. Montreal Cognitive Assessment w as used to evaluate the cognitive function at three month after onset. Multivariate logistic regression analysis w as used to identify the relationship betw een the coefficient of variation of blood pressure w ithin 7 days and the cognitive impairment at 3 months after onset. Results A total of 708 patients w ith acute ischemic stroke w ere enrol ed in the study. At 3-month folow-up, 510 patients (72.0%) had cognitive impairment and 198 (28.0%) had normal cognitive function. The coefficient of variation for systolic blood pressure ( 8.3 ±1.2 vs.8.7 ±1.4; t= -3.299, P=0.001) and coefficient of variation for diastolic blood pressure ( 7.8 ±1.3 vs.8.0 ±1.5; t= -2.529, P=0.012) in the cognitive impairment group w ere significantly higher than those in the normal cognitive function group. With the first quintile as a reference, after adjusting other confounding factors, multivariate logistic regression analysis show ed that cognitive impairment at 3 months after onset w as significantly associated w ith coefficient of variation for systolic blood pressure. The odds ratios and 95 % confidence intervals for the 2-5 quantile groups w ere 2.33 (1.18-4.6), 2.31 (1.15-4.66), 2.70 (1.29-5.65), and 4.82 (1.92-12.1), respectively ( al P<0.05 ). Conclusion Systolic blood pressure variability in the acute phase of ischemic stroke is associated w ith cognitive impairment.
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ObjectiveToinvestigatethecorrelationbetweentheetiologicsubtypeandoutcomein patients w ith non-disabling ischemic cerebrovascular events (NICE). Methods The consecutive patients w ith NICE admitted to hospital within 7 days after onset were enroled prospectively and folowed for 90 days. Etiologic subtypes w ere classified according to the Chinese Ischemic Stroke Subclassification (CISS). Good outcome w as defined as modified Rankin Scale score 0-2. Multivariate logistic regression analysis w as used to identify the independent risk factors for stroke recurrence and poor outcomes. Results A total of 162 patients with NICE were enroled. According to CISS, 76 (46.9%) were classified into large artery atherosclerosis (LAA), 54 (33.3%) into penetrating artery disease (PAD), 15 (9.3%) into cardiogenic stroke (CS), 11 (6.8%) into undetermined etiology (UE), and 6 (3.7%) into other etiology (OE). A total of 30 patients (18.5%) had recurrent stroke w ithin 90 days and 42 (25.9%) had poor outcomes. The proportions of patients w ith diabetes (46.7%vs.20.5%;χ2 =8.885, P=0.003), previous stroke or transient ischemic attack (46.7%vs.25.0%;χ2 =5.572, P=0.018), CS (20.0%vs.6.8%;Fisher exact test:P=0.036) in the stroke recurrence group w ere significantly higher than those in the non-stroke recurrence group, and the proportion of PAD patients in the stroke recurrence group w as significantly low er than that in the non -stroke recurrence group ( 16.7%vs.37.1%; χ2 =4.602, P=0.032 ). Multivariate logistic regression analysis show ed that diabetes (odds ratio [OR] 2.137, 95%confidence interval [CI] 1.359-4.187;P=0.004) and CS (OR 5.236, 95%CI 2.326-10.256; P<0.001) w ere the independent risk factors for recurrent stroke of NICE. The proportions of patients w ith hypertension ( 83.3%vs.61.7%; χ2 =6.635, P=0.010 ), diabetes (40.5%vs.20.0%;χ2 =6.900, P=0.009), atrial fibrilation (35.7%vs.14.2%;χ2 =9.113, P=0.003) and CS ( 19.0%vs.5.8%; Fisher exact test: P= 0.017 ) in the poor outcome group w ere significantly higher than those in the good outcome group, and the proportion of PAD patients ( 16.7%vs. 39.2%;χ2 =7.088, P=0.008) in the poor outcome group w as significantly low er than that in the good outcome group. Multivariate logistic regression analysis show ed that diabetes ( OR 2.257, 95%CI 1.209-3.687; P=0.010), atrial fibrilation (OR 3.137, 95%CI 1.359-6.107, P=0.002), and CS (OR 6.123, 95%CI 2.026-12.256, P<0.001) w ere the independent risk factors for poor outcomes in patient w ith NICE. Conclusions The etiologic subtype is associated w ith the poor outcomes and recurrent stroke, and can provide reference for recurrence and clinical outcome assessment in patients w ith NICE.
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ObjectiveToinvestigatetheriskfactorsforunfavorableoutcomeinpatientswithminor ischemic stroke. Methods Patients with minor ischemic stroke were enroled prospectively. The modified Rankin Scale ( mRS ) w as used to assess the clinical outcome at day 90 after onset, and mRS 0-2 w as defined as favorable outcome. The demographic data, vascular risk factors, clinical data, imaging data, stroke etiologic subtypes, laboratory test results, and treatment methods in the favorable outcome group and unfavorable outcome group w ere compared. Multivariate logistic regression analysis w as used to identify the independent risk factors for early poor outcome in patients w ith minor ischemic stroke. Results A total of 516 patients with minor ischemic stroke were enroled. At day 90 after onset, 90 patients (17.44%) had unfavorable outcome and 426 (82.56%) had favorable outcome. Multivariate logistic regression analysis showed that age (odds ratio [OR] 1.045, 95% confidence interval [CI] 1.017-1.074; P=0.002), heart diseases (OR 2.021, 95%CI 1.063-3.841; P=0.032), baseline National Institutes of Health Stroke Scale (NIHSS) score (OR 1.662, 95%CI 1.177-2.347; P=0.004), limb movement disorder ( OR 2.430, 95%CI 1.010-5.850; P=0.048), ataxia (OR 2.929, 95%CI 1.188-7.221;P=0.020), early neurological deterioration ( OR 50.994, 95%CI 17.659-147.258; P<0.001), infarct diameter ( OR 1.279, 95%CI 1.075-1.521; P=0.005), non-responsible vascular stenosis ( OR 2.518, 95%CI 1.145-5.536;P=0.022), and large artery atherosclerotic stroke ( OR 2.010, 95%CI 1.009-4.003; P=0.047) w ere the independent risk factors for unfavorable outcome in minor ischemic stroke. Conclusions The early poor outcome of minor ischemic stroke is closely associated w ith age, heart diseases, baseline NIHSS score, limb movement disorder, ataxia, early neurological deterioration, infarct diameter, non-responsible vascular stenosis, and large artery atherosclerotic stroke. The relevant examinations need to be improved early, the etiologic subtype should be identified, and the correct clinical treatment should be guided.
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ObjectiveToinvestigatetheprotectiveeffectandmechanismofscutelarincombinedwith paeoniflorin after permanent cerebral ischemia in rats. Methods Forty-eight adult male SD rats w ere randomly divided into four groups: sham-operation, cerebral ischemia, scutelarin+ paeoniflorin, and cyclopamine (n=12 in each group). A model of permanent middle cerebral artery occlusion w as induced by suture method. The intraperitoneal injection of cyclopamine 6 mg/kg, a specific inhibitor of sonic hedgehog (SHH) pathw ay, at 15 min before ischemia in the cyclopamine group, w hile other groups w ere intraperitoneal y injected an equal volume of saline. At 0 hour and 3 hours after ischemia, the scutel arin+paeoniflorin group and cyclopamine group w ere intraperitoneal y injected scutel arin ( 20 mg/kg ) and paeoniflorin (30 mg/kg), while other groups were intraperitonealy injected an equal volume of saline. Neurological deficit scores w ere performed at 24 hours after ischemia, and then the rats w ere decapitated. The cerebral infarct volume w as measured by using 2,3,5-triphenyltetrazolium chloride (TTC) staining. Real-time fluorescent quantitative polymerase chain reaction and Western blotting w ere used respectively to detect the expression levels of SHH, Patched-1, Gli-1 mRNAs and proteins in the ischemic cortex. Results The neurological deficit scores in the cerebral ischemia group, scutel arin+paeoniflorin group, and cyclopamine group w ere 3.33 ±0.52, 1.50 ±0.55, and 3.67 ±0.52, respectively. The neurological deficit score in the scutel arin+paeoniflorin group w as significantly low er than that in the cerebral ischemia group ( P<0.05), and the neurological deficit score in the cyclopamine group w as significantly higher than that in the scutelarin+paeoniflorin group ( P<0.05). The infarct volume percentage in the cerebral ischemia group, scutelarin+paeoniflorin group, and cyclopamine group were 31.77%±1.19%, 22.94%±2.65%, and 35.53%±0.20%, respectively. The infarct volume in the scutel arin+paeoniflorin group w as significantly less than that in the cerebral ischemia group ( P<0.05), and the infarct volume in the cyclopamine group was significantly larger than that of the scutelarin+paeoniflorin group (P<0.05). The expression levels of SHH, Patched-1, Gli-1 mRNAs and proteins in the cerebral ischemia group, scutelarin+paeoniflorin group, and cyclopamine group w ere significantly higher than those in the sham -operation group (al P<0.05). The expression levels of SHH, Patched-1, Gli-1 mRNAs and proteins in the scutelarin+paeoniflorin group were significantly higher than those in the in the cerebral ischemia group (al P<0.05), and the expression levels of Gli-1 mRNA and protein in the cyclopamine group were significantly lower than those in the scutelarin+paeoniflorin group ( al P<0.05 ). Conclusions The scutel arin combined w ith paeoniflorin has certain protective effect on focal cerebral ischemia injury in rats. Its mechanism is associated w ith the activation of SHH signaling pathw ay.
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ObjectiveToinvestigatetheeffectsofcaveolin1(Cav1)onexpressionsofproinflammatory cytokine interleukin (IL)-1βand IL-6 in the ischemic cortex after permanent middle cerebral artery occlusion in mice. Methods The Cav-1 knockout mice (n=40) and wild-type mice (n=40) were randomly divided into ischemia groups and sham operation groups (n=20 in each group). They w ere also redivided into ischemia or sham operation at 3, 7, 10 and 14 d time points ( n=5 in each time point). A permanent middle cerebral artery occlusion model w as induced by the suture method. Immunohistochemical method w as used to detect the expressions of IL-1βand IL-6 in the ischemic cortex. Results The expression levels of IL-1βand IL-6 in the ischemic cortex at each time point in the ischemia group in Cav1 knockout mice w ere significantly higher than those in the ischemia group in the w ild-type mice ( al P< 0.05 ). Conclusions The upregulations of proinflammatory cytokines IL-1βand IL-6 in the ischemic cortex in Cav1 knockout mice suggests that Cav1 plays an important role in aleviating inflammation after cerebral ischemia.
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ObjectiveToinvestigatetheeffectofserumuricacid(SUA)levelonshort-term outcomes of recombinant tissue plasminogen activator (rtPA) for intravenous thrombolysis in patients w ith ischemic stroke. Methods The patients w ith acute ischemic stroke treated w ith intravenous rtPA thrombolysis w ere enrol ed. The demographic data, clinical data, and laboratory parameters w ere compared and analyzed according to the modified Rankin scale (mRS) scores at discharge. A good outcome was defined as a 3-month mRS score of 0 in patients w ith a baseline National Institute of Health Stroke Scale (NIHSS) score≤7, a score of 0–1 in those w ith a baseline NIHSS score of 8-14, and a score of 0–2 in those w ith a baseline NIHSS score ≥ 15. Results A total of 108 patients w ith acute ischemic stroke treated w ith intravenous rtPA thrombolysis w ere enrol ed. There w ere 66 patients (61.11%) in the good outcome group and 42 (38.89%) in the poor outcome group. The constituent ratios of age (62.21 ±10.25 years vs. 57.83 ±10.457 years; t=2.138, P=0.035), the baseline NIHSS scores (median and interquartile range, 10 [8-12] vs.4 [3-7]; Z=5.537, P<0.001), type 2 diabetes mel itus (40.48%vs.12.12%; χ2 =11.600, P=0.001), and previous history of stroke (9.52%vs.9.09%;χ2 =4.366, P=0.037) of the poor outcome group w ere significantly higher than those of the good outcome group, w hile the SUA level (323.119 ±87.869 mmol/L vs.385.961 ±76.166 mmol/L; t=3.936, P<0.001) w as significantly low er than that of the good outcome group. Multivariate logistic regression analysis show ed that the previous history of diabetes melitus type 2 (odds ratio [OR] 5.471, 95%confidence interval [CI] 1.472-20.334;P=0.011) and higher baseline NIHSS score (OR 1.306, 95%CI 1.147-1.486; P<0.001) were the independent risk factor for short-term clinical outcomes, w hile higher SUV level ( OR 0.992, 95%CI 0.986-0.998; P=0.015) w as an independent protective factor for poor short-term outcome. Conclusions The increased SUA level is an independent protective factor for good short-term outcome in patients treated w ith intravenous rtPA.
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ObjectiveToinvestigatetherolesofbrain-derivedneurotrophicfactor(BDNF)and tyrosine receptor kinase B (TrkB) in ischemic postconditioning. Methods Wistar rats w ere randomly assigned to three groups:a sham operation (9 rats), an ischemic postconditioning, and an ischemia-reperfusion group. According to the reperfusion time, the latter 2 groups w ere redivided into 6, 12, 24, 48, and 72 h subgroups (9 rats in each subgroups). A middle cerebral artery occluded by suture method for a cerebral ischemia-reperfusion model. Triphenyl tetrazolium staining w as used to detect infarct volume (P=4). Immunohisto-chemical staining w as used to detect the expression levels of BDNF and TrkB proteins (P=5). Results The infarct volumes in the ischemic postconditioning group w ere reduced significantly compared w ith those in the ischemia-reperfusion group (6 h:143.3 ±8.7 mm3 vs.166.8 ±7.5 mm3, t=4.104, P=0.006;12 h:151.7 ±7.8 mm3 vs.171.6 ±9.1 mm3, t=3.314, P=0.016; 24 h: 159.2 ±9.3 mm3 vs.177.1 ± 7.6 mm3, t=3.000, P=0.024;48 h:166.9 ±9.6 mm3 vs.184.9 ±9.0 mm3, t=2.732, P=0.034;72 h:172.0 ±9.1 mm3 vs.198.1 ±8.2 mm3, t=2.640, P=0.039), and the positive cel numbers of BDNF (6 h:23.98 ±4.07 vs.18.63 ±2.5, t=2.479, P=0.038;12 h:27.64 ±3.18 vs.22.01 ±3.14, t=2.817, P=0.023;24 h:34.82 ±4.17 vs.28.46 ±4.05, t=2.446, P=0.040; 48 h:34.30 ±3.27 vs.26.29 ± 3.26, t=3.872, P=0.005;72 h:28.77 ±3.53 vs.23.64 ±3.54, t=2.297, P=0.051) and TrkB (6 h:33.83 ±3.90 vs.21.51 ±3.86, t=5.012, P<0.001; 12 h:38.59 ±4.84 vs.23.41 ±3.67, t=5.586, P<0.001;24 h:46.07 ±3.06 vs.28.78 ±3.61, t=8.169, P<0.001; 48 h:47.90 ±3.30 vs.29.51 ± 3.81, t=8.160, P<0.001; 72 h:42.78 ±4.07 vs.27.46 ±3.19, t=6.623, P<0.001) per high-pow er field at each time point in the ischemic postconditioning group w ere significantly more than those in the ischemia-reperfusion group. Conclusions Ischemic postconditioning upregulates the expressions levels of BDNF and TrkB proteins after ischemia-reperfusion and reduces cerebral infarct volumes. BDNF/TrkB may play an important neuroprotective effect in ischemic postconditioning.
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Hemorrhagictransformation(HT)referstointracerebralhemorrhageoccurredwhenthe blood vessels restore blood flow after acute ischemic stroke. It is one of the common complications of ischemic stroke. HT may not have any clinical manifestations and can also be manifested as limb paralysis aggravation, decreased consciousness level, and other symptoms. The symptomatic HT may result in prolonged hospitalization, increased disability and fatality. Therefore, research on the mechanisms and risk factors for HT may be expected to provide the basis for clinical treatment, and thus improve the prognosis of patients. This article review s the formation mechanism of HT, risk factors, screening of high-risk patients, and prevention and treatment.
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Cerebralischemiacaninducecelnecrosisincoreoftheinfarction,andapoptosisinthe ischemic penumbra. The mitogen-activated protein kinases (MAPKs) signaling pathw ays are activated after cerebral ischemia, causing programmed cel death, including apoptosis. This article review s the relationship betw een the MAPKs signaling family and neuronal apoptosis after cerebral ischemia.
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Inrecentyears,somecardiovascularguidelineshavegradualyintroducedambulatory blood pressure monitoring ( ABPM ) as an indispensable means for better diagnosis and management of hypertensive patients. ABPM can more comprehensively provide 3 types of information that has potential clinical value:the assessment of real or mean blood pressure level, the diurnal rhythm of blood pressure, and the blood pressure variability. This article review s the roles of ABPM in the outcome assessment in patients w ith acute ischemic stroke.
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Althoughtheevidenceoftheevidence-basedmedicinehasshowedthatrecombinant tissue-type plasminogen activator can effectively open the occluded vessels, because of its short therapeutic time w indow and the risk of bleeding, the thrombolytic rate is general y low er currently. Clinical studies have show ed that telestroke can effectively shorten the treatment time of the patients, increase the thrombolytic rate, reduce the risk of bleeding, and improve the outcomes of patients. Although the application of telestroke is restricted in many w ays, such as technology, policy, and funding, w ith the grow ing maturity of the related technologies, telestroke w il play an increasingly important role in the treatment of stroke.
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ObjectiveToinvestigatethecorrelationofaspirinresistance(AR),genepolymorphismof platelet membrane glycoprotein (GP)Ⅱb HPA-3 and recurrent ischemic stroke. Methods The consecutive patients w ith acute ischemic stroke and gender, age-matched healthy subjects w ere enrol ed. Adenosine diphosphate (ADP) and arachidonic acid (AA) w ere used as inducing agents. The platelet aggregation rate (PAgT) was detected by flow cytometry. AR was defined as PAgTADP≥39.27% and PAgTAA≥34.27%. Polymerase chain reaction-restriction fragment length polymorphism w as used to detect the GPⅡbHPA-3 genotype. Results A total of 224 patients w ith acute ischemic stroke (case group) and 98 healthy subjects (control group) were enroled. In the case group, 162 patients had the first-ever stroke (first-ever stroke group) and 62 had recurrent stroke (recurrent stroke group). The incidence of AR in the case group w as 15.18%, in w hich the incidence of AR in the recurrent group w as significantly higher than that in the first-ever stroke group (27.42%vs.10.49%; χ2 =9.977, P=0.002). The frequencies of bb genotype ( P=0.004) and b alele (P=0.001) in the recurrent group were significantly higher than those in the first-ever stroke group. In the case group, the frequencies of bb genotype ( P=0.028) and b alele (P=0.004) in the AR group w ere significantly higher than those in the non-AR group. Multivariable logistic regression analysis show ed that AR (odds ratio [OR] 2.933, 95%confidence interval [CI] 1.326-6.486;P=0.008) and bb genotype (OR 2.198, 95%CI1.164-4.149, P=0.015) w ere the independent risk factors for recurrent ischemic stroke. Conclusions AR and GP Ⅱb HPA-3 bb genotype are associated w ith recurrent ischemic stroke.
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Objective To investigate the correlation between lipoprotein-associated phospholipase A2 (Lp-PLA2) gene R92H polymorphism and ischemic stroke and its subtype in a Chinese Han population of Shandong province. Methods A total of 386 patients w ith first-ever ischemic stroke and 368 healthy controls in China Shandong region w ere enrol ed. According to the TOAST criteria, the patients w ere further divided into large artery atherosclerosis (LAA) and smal artery occlusion (SAO). Enzyme linked immunosorbent assay w as used to detect the serum Lp-PLA2 level. Polymerase chain reaction and directly sequencing w ere used to detect R92H gene polymorphism. Results The serum Lp-PLA2 levels in the ischemic stroke group, LAA group and SAO group w ere higher than that in the control group, and there w ere significant differences (al P<0.01). The distribution frequencies of GA (P=0.006), AA (P=0.020), AA+AG (P=0.009), and A al ele (P=0.001) in the ischemic stroke group w ere significant higher than those in the control group. There w ere also significant differences in distribution frequencies of GA+AA genotype (P=0.007) and A al ele (P<0.001) betw een the LAA group and the control group, w hile the SAO group w as not the case. Multivariate logistic regression analysis showed that GA+ AA genotype (odds ratio [OR] 1.43, 95%confidence interval [CI] 1.02-2.00; P=0.029), GA genotype (OR 1.42, 95%CI 1.01-2.00; P=0.037), and A alele (OR 1.44, 95%CI 1.11-2.18; P=0.028) were the independent risk factors for ischemic stroke. GA+AA genotype (OR 1.73, 95%CI 1.18-2.55; P<0.001) and GA genotype (OR 1.67, 95%CI 1.13-2.48; P<0.001) w ere the independent risk factors for LAA, and they w ere not significantly independent correlated w ith SAO. Conclusions The serum Lp-PLA2 levels increased in patients w ith ischemic stroke, and they increased most significantly in the LAA group. The R92H gene polymorphism might be associated w ith the susceptibility of ischemic stroke in a Chinese Han population of Shandong province.
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Necroptosisisanewlydiscoveredwayofceldeath.Itisassociatedwithinfection, tumor, heart disease, neurodegenerative disease, cerebrovascular disease, and other diseases. Necroptosis involves in the occurrence and development of cerebral ischemia-reperfusion injury. Therefore, w hen the cerebral ischemia is studied in depth, the induction, regulation and blocking mechanisms of necroptosis are not only conducive to deepen the understanding of the death mode of brain cel s, but also conducive to develop new drugs for the new targets in the treatment of cerebral ischemia.
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Subclinicalhypothyroidism(SCH)maybeassociatedwithcarotidatherosclerosis, dyslipidemia, hypertension, hyperhomocysteinemia, and coronary heart disease, and these factors are often regarded as the risk factors for ischemic stroke. The correlation betw een SCH and the risk of stroke remains unclear now . The hypothesis of SCH increasing the risk of stroke has not been confirmed. Even studies have show n that SCH may have a beneficial effect for the prognosis of stroke. This article review s the relationships betw een SCH and risk factors for stroke, and risk of stroke and prognosis.
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Sleep-disorderedbreathingarecloselyassociatedwithischemicstroke.Sleep-disordered breathing includes obstructive sleep apnea and central sleep apnea. Studies have show n that obstructive sleep apnea is an independent risk factor for stroke, w hile stroke can also increase the incidence of sleep-disordered breathing. This article review s the latest research progress of sleep-disordered breathing and stroke.
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Endothelialprogenitorcels(EPCs)arethepluripotentstemcelsofvascularendothelial cels. They have self-differentiation and proliferation ability. A large number of animal experiments and preliminary clinical studies have show n that EPCs have broad prospects of clinical application. This article review s the research status of EPCs and their application in the clinical treatment of ischemic stroke.
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Ambulatorybloodpressuremonitoring(ABPM)providesmoreextensiveclinical information than clinical casual blood pressure. It can effectively identify w hite coat hypertension and masked hypertension and is superior to clinical casual blood pressure in predicting stroke risk. Both daytime and nighttime systolic blood pressures are the independent predictors of stroke, and the predictive value of nighttime systolic blood pressure is higher. In addition, ABPM can also be used to evaluate the blood pressure response and control during the primary and secondary stroke prevention. This article review s the application of ABPM in stroke prevention.
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Objective ToobservetheeffectsofNaokangⅡ,atraditionalChinesemedicineon spatial learning and memory abilities and hippocampal neurogenesis in rats with cerebral ischemia. Methods Atotalof54SDratsweredividedinto6groupsaccordingtothedigitalrandommethod:a control,a sham operation,a model,a low-dose,a medium-dose,and a high-dose NaokangⅡ group (the low-,medium-,and high-dose groups were 5,10,and 20 times of adults (n=9 in each group). A rat model was induced by ligate the bilateral common carotid arteries permanently. The bilateral common carotid arteries were only isolated but not ligated in rats of the sham operation group. The rats in the control group were not given any treatment. After modeling,the rats in the treatment groups were treated with NaokangⅡ. The rats in the control,sham operation,and model groups were given equal volume of isotonic saline (2 ml). Morris water maze test and space search experiment were used to evaluate the learning and memory abilities in rats 9 weeks after modeling. Immunofluorescence staining and immunohistochemical methods were used to observe proliferation and differentiation of neural stem cells (NSCs). Western blot was used to detect the expression of autophagy related protein Beclin-1 and LC-3Ⅱ. Results (1 )The escape latencies of the model group from 1 to 5 days were 100 ± 13,98 ± 13,82 ± 14,72 ± 15,and 46 ± 7 s,respectively. They were significantly longer than those of the sham operation group and the control group (all P<0. 05). The search distances were 1239 ± 127,1011 ± 122,959 ± 123,553 ± 66,and 407 ± 29 cm,respectively. They were significantly increased as compared with those of the sham operation group and control group (all P<0. 01). Both the escape latencies and search distances of the rats in the Naokang Ⅱ low-,medium-,and high-dose groups were significantly shorter than those of the model group (P<0. 05). The escape latencies on the fifth day were 20 ± 6,19 ± 8,and 15 ± 6 s,respectively,and the search distances were 234 ± 38, 297 ± 23,and 99 ± 22 cm,respectively. Nine weeks after modeling,the quadrant search time on the original platform in the rats of the model group was 30 ± 9 s,it was significantly shorter than that of the sham operation group (P<0. 01). The quadrant search time on the original platform of the Naokang Ⅱ low-, medium-,and high-dose groups were 34 ± 6,38 ± 8,and 40 ± 10 s,respectively. They were significantly longer than those of the model group (P <0. 01). (2)Nine weeks after modeling,the results of immunofluorescence and immunohistochemistry showed that the number of BrdU-positive cells and the Nestin positive cells in hippocampal dentate gyrus of the model group were higher than those of the control group and the sham operation group (P<0. 05). The number of BrdU-positive cells and Nestin positive cells of Naokang Ⅱ each dose group were significantly higher than those of the model group (P<0. 05). The expression of LC-3Ⅱand Beclin-1 in the model group was significantly higher than those in the control and sham operation groups (P<0. 01). The expression of LC-3Ⅱ in the medium- and high-dose groups was 143 ± 9 and 129 ± 9 respectively,and the expression of Beclin-1 was 139 ± 10 and 124 ± 7 respectively, andtheyweresignificantlylowerthanthemodelgroup(P<0.01).Conclusion NaokangⅡcanimprove the cognitive function in rats with cerebral ischemia,promote neurogenesis in the dentate gyrus,and inhibit autophagic cell death.
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Objective To assess the applied value of proton magnetic resonance spectroscopy(1HMRS) in evaluating the canine model of acute ischemic cerebral damage and intra-arterial thrombolytic therapy.Methods 18 adult hybrid canines were all occluded with self-thromboses and randomly divided into 6 groups(three canines in each group),group B1,B3,B6,B9 and B12 were given intra-arterial thrombolytic therapy with urokinase(10,000IU/kg) at 1.5,3.5,6.5,9.5 and 12.5 hours after embolism respectively.The axial diffusion-weighted images(DWI) and 1HMRS were performed in all canines at 1,3,6,9,12 and 24 hours after embolism respectively.24 hours after embolism,one canine in every group was randomly selected to be executed pathologic examination.Results NAA,Cho and Cr decreased in non-thrombolytic group,specially NAA in the first 6 hours.Cho and Cr decreased a little,but they were not so significant compared with NAA.The relative value of Lac was persistent elevation within 24 hours.In thrombolytic group,the degree of elevation of Lac was significantly smaller than in group A(P