Cerebral vasospasm (Cerebral Vasospasm CVS) is one of the most serious complications of subarachnoid hemorrhage (subarachnoid hemorrhage SAH). The incidence is as high as30%to90%. It often causes serious local brain tissue ischemia or delayed ischemic brain injury, an important cause of death and disability of SAH patients. But the pathogenesis is not yet clear. Studies suggest that in recent years the inflammatory response plays an important role in the pathogenesis of delayed cerebral vasospasm, and possible mechanisms include systemic inflammatory response, leukocytes and endothelial cell interactions, a variety of cytokines, adhesion molecules and signal transduction pathways participate in certain inflammatory protein genotype change. Cytokines are a class of small molecular weight of the soluble protein, secreted by immune system cells and other cell types,which can promote interaction between cells and other biological activity. The study shows that the mutual regulation with the cascade of inflammatory cells between cytokines in the process of vascular spasm amplification vasospasm important factor. Large number of studies reported in the extracellular matrix of multiple molecules involved in the destruction and reconstruction of the blood-brain barrier, neurons necrosis and repair process, affecting the development and prognosis of the disease, and its activity changes brain microvascular permeability, blood-brain barrier collapse invasion of inflammatory cells and brain edema. Decorin (Decorin, DCN) is a leucine-rich proteoglycan small molecule which is important mediators of the extracellular matrix (Extracellular Matrix, ECM), having a variety of biological activity. DCN in the regulation of cell adhesion, migration, proliferation, collagen fiber formation and plays an important role in the regulation of activity of transforming growth factor (Transforming growth factor-β1TGF-β1). Recent studies found that the decorin can up-regulate expression of TGF-1and interleukin hormone (IL-1) of the horizontal lower, but down-regulate that of IL-4and tumor necrosis factor (TNF-a) levels, suggesting DCN regulation of cytokine production plays an important role. DCN participate in brain tissue extracellular matrix remodeling, and regulation of apoptosis and regeneration of brain microvascular endothelial cells, and it may be directly or indirectly involved in vasospasm and delayed cerebral damage our previous study in rat whole genome microarray studies found the pathophysiological process. Last DCN basic research also showed that more of the active medium have a direct role in the DCN and extracellular matrix. Studies have shown that DCN level in the plasma of acute ischemic stroke patients was significantly lower than the control group, and2weeks after the onset of was dynamically reduce their levels of MMP-2concentrations were positively correlated, and the concentration in the different clinical hypotype change differences. Thus, we suggest that the DCN the Collaborative the other cytokines directly or indirectly involved in the inflammatory response after subarachnoid hemorrhage, and eventually lead to the occurrence of vasospasm and delayed cerebral damage pathophysiological process, which may regulate inflammatory cytokines The extracellular matrix reconstruction ischemia at the role of vasospasm, neuronal repair play a role in regulating. This study by case-control study observed DCN and cytokines (TGF-β1, TNF-a, MMP-2, MMP-9) concentration in plasma and cerebrospinal fluid of patients with acute SAH change its cerebral vasospasm and prognosis Related to clarify its role in the diagnosis of vasospasm, to provide new ideas for vasospasm after SAH disease prevention, treatment and prognosis of rehabilitation.[Methods] cytokines are measured by enzyme-linked immunosorbent assay (ELISA) the acute SAH vasospasm group and the control group (the acute SAH non-spasm group) at different time points after onset (<3days,4-7days,8-14days) dynamic observed hypersensitivity CRP the DCN and cytokines (TGF-bl, TNF-a, MMP-2, MMP-9), the dynamic trend analysis of high-sensitivity CRP, the DCN and cell factor (TGF-β1, TNF-a, MMP-2, MMP-9) whether vasospasm and non-vasospasm group differentially expressed, and after3months of telephone follow-up of2groups of patients prognosis (mRS score). Further clarify the indicators whether the differentially expressed in different prognosis of patients.[Results]Hs-CRP (spider blood serum after1-3days, P=0.041) the DCN (spider blood after8-12days P=0.003), TGF-β (spider blood after8-12days P=0.049) as well as TNF-a (spider blood after4-7days P=0.01) and vasospasm. In addition, mean concentration of TGF-β, serum CRP, DCN, TNF-a, of MMP-2, MMP-9in the spasm groupare higher than in non spasm group.Hs-CRP in cerebrospinal fluid of (spider blood after1-3days, P=0.011, spider blood after4-7days P=0.001), DCN (8-12days after the spider blood P=0.037), TGF-β (spider1-3days after blood, P=0.0482, spider blood4-7days after P=0,003) related to vasospasm. In addition to TGF-P in4-7days after SAH specimens, cerebrospinal fluid CRP, DCN, TNF-a, of MMP-2, MMP-9concentration mean in the spasm group than in non spasm group.3, between prognosis (Mrs<2) and bad (Mrs>2) grouping, serum the DCN (spider blood after1-3days P<0.001), MMP-2(spider blood after4-8days P=0.045, spider blood8-12 days after P=0.05), as well as TNF-a (spider blood after4-7days P=0.001spider blood after8-12days P=0.05) related SAH prognosis.Between good prognosis (Mrs<2) and bad (Mrs>2) grouping, I Is-CRP in cerebrospinal fluid (spider blood after4-7days P=0.011) the DCN (spider blood after1-3days, P<0.043, spider blood after4-7days P<0.04) and MMP-9(spider blood after1-3days, P=0.011) and the prognosis of SAH.5, Logistic regression analysis indicated that the cerebrospinal fluid in the DCN (p=0.024), CRP (P=0.034), content and fisher (P=0.014) grading as a predictor of acute subarachnoid hemorrhage independent prognostic factors.6. the receiver operating characteristic curve (ROC) analysis showed that DCN level for the diagnosis of ischemic stroke occurred significant (p<0.01), and select the DCN<8500pg/ml as the diagnosis of ischemic stroke diagnostic industry value point, the sensitivity was79.4%, specificity of62.8%. Logistic regression analysis showed that DCN<8500pg/ml is an independent risk factor for ischemic stroke (OR=4.8;95%Cl:2.1-11.1; p<0.01).Conclusion In this study, case-control found the acute SAH plasma and cerebrospinal fluid of DCN and other inflammatory cytokines CVS group somewhat higher than those in the control group different expression than the prognosis good group P piece in the poor prognosis group. This suggests that the inflammatory cytokines directly or indirectly involved in the pathophysiology of vasospasm and delayed brain damage, and inflammatory factors that may exist between the interaction. Extracellular matrix reconstruction, neurons repair play a role in regulating the possible interaction between the regulation of inflammatory cells and delayed brain damage after hemorrhage. DCN and other cytokine levels change can help the diagnosis. prognosis and treatment of vasospasm after SAH. |