Research On The Association Of The Serum Concentration Of Gal-3 With Atherosclerosis In Patients With Acute Ischaemic Infarcts And Subcortical Arteriosclerotic Encephalopathy

Objective:Galectin-3, a marker of macrophage activation, may be instrumental in the formation of plaque and participate in the progression of atherosclerotic lesions, leading to plaque repture and thrombosis. The study was to investigate the expression levels of galectin-3 in patients of acute ischemic stroke and subcortical arteriosclerotic encephalopathy(SAE),combining with multiple risk factors of cerebral vascular disease and inflammatory index of Hypersensitivity C reactive protein(Hs-CRP), to analyze the relationship between stabilaty of carotid plaque and atherosclerotic lesion.Methods:We enrolled hospitalized patients by acute ischaemic infarcts(90 case) and subcortical arteriosclerotic encephalopath(25 case) as research object. According to carotid artery ultrasound, the patients with acute stroke were selected for three groups(unstable plaque, stable plaque,no plaque). Control group included 30 subject with matched age and sex frequencies who were histopathologically confirmed to be without stroke performance and carotid artery plaque. The clinical data, such as age, sex,hypertension, and smoking, was collected. The most important traditional risk factors,such as blood sugar, blood fat, homocysteine, hypersensitive c-reactive protein, were detected. Plasma Gal-3 was quantified using an ELISA kit. The serum indexes in different groups were analyzed by the T-test, Chi-square test and Mann-Whitney U.Analyzed the connection of the Galectin-3 and other indexes to plaques and SAE through multiple Logistic regression analysis.Results:1.The serum concentration of Galectin-3 in SAE(5973.47±484.62 pg/ml) were significantly higher than that of normal controls(2971.90±322.33 pg/ml), the difference was obvious significant(P<0.01).The univariate analysis showed that Glu?TC?LDL-C?Hs-CRP?t-HCY?Gal-3 was related with the occurrence of Binswanger Disease. Introduced the factors above in the multiple lodistic regression model found that Glu ? Hs-CRP ?t-HCY?Galectin-3 were important risks of SAE.2.Different plaque stability in acute ischaemic infarcts, the serum levels of Galectin-3 at different, the difference was obvious significant(P<0.01). The Galectin-3level in the unstable plaque group was the highest(7636.06±754.19 pg/ml), stable plaque group was second(5125.14±427.58 pg/ml), no plaque group was the lowest(4024.76±403.92 pg/ml). By the univariate analysis, the formation of unstable plaques were correlated with TC?TG?LDL-C?Hs-CRP?t-HCY?Gal-3. In multivariate logistic regression analysis, the serum concentration of LDL-C?HsCRP?Galectin-3 were factor for unstable CAS plaques.Conclusion:1. Inflammatory cytokine of Galectin-3 and Hs-CRP may influence in the occurrence and development of SAE.But whether it be the therapeutic targets of SAE wait to be proved.2. The serum concentration of Gal-3 degrees vary with plaque of carotid artery,which is expected to be inflammatory predictor of plaque stability. The marker of Gal-3may be used in screening the high risk population of stroke, guiding risk stratification.