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R (G-CSF) (F9, F10) had appeared 6 h post-CLP and C-X-C chemokine receptor type 4 (CXCR4) (E7, E8) had appeared 24 h post-CLP (Figure 6F). Therefore, TSP, PF4, TIMP-1and TCK-1 warrant evaluation as biomarkers of the early stage of sepsis-induced DIC. The protein microarray signal intensities of these cytokines and chemokines over time are summarized in Figure 7. TSP levels in the CLP group increased and peaked sharply at 1h post-CLP; they then decreased gradually until 72 h post-CLP, but remained significantly higher than in the sham group (n = 5, p < 0.05). PF4 levels in the CLP group were increased 1 h post-CLP, peaked at 2 h post-CLP (n = 5, p < 0.05), then decreased rapidly to the level of the sham group (n = 5, p > 0.05). TIMP-1 levels were also increased 1 h post-CLP, then continued to increase in the CLP group (n = 5, p < 0.05). TCK-1 levels in the CLP group were significantly increased 2 h post-CLP and remained higher than in the sham group until 72 h post-CLP (n = 5, p < 0.05). Somewhat differently, the serum levels of TIMP-1 measured by ELISA were also increased 2 h post-CLP significantly (n = 5, p < 0.05). Nevertheless, the serum levels of TSP, TIMP-1 and TCK-1 measured by ELISA have the similar change with the protein microarray signal intensities analysis (n = 5, p < 0.05, Figure 8).Discussion As one of the most severe complications of sepsis, DIC is always associated with poor prognosis, multiply organ dysfunction and high mortality. Generally, clinical diagnosis of DIC relies on platelet count, coagulation assay, d-dimer and fibrinogen. However, when the results of such tests are positive, the best time for treatment had already passed. In much basic research, the difficulty of early prediction of sepsis-induced DIC is related to the large number of coagulation factors, chemokines and cytokines, and their complicated Methyl 5-amino-2,4-difluorobenzoate interactions. Plateletderived factors are distinct from others because of their role at the crossroads of coagulation and inflammatory pathways such as the complement, contact phase, coagulation and fibrinolytic systems, host defense and antibacterial action [29,30]. Protein microarray technology allows us to study many molecules simultaneously and elucidate their interactions. A protein-detecting microarray comprises many different affinity reagents arrayed at high density. 4,4,5,5-Tetramethyl-2-(2-methylprop-1-en-1-yl)-1,3,2-dioxaborolane Each agent captures a target protein from a complex mixture, and the captured proteins are subsequently detected and quantified [31,32]. For the present study, a protein microarray kit was customized to serially detect fifty platelet-secreted PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/15957913 factors in a mouse CLP model. The CLP model imitates sepsis by creating a bowel perforation with leakage of fecal material into the peritoneal cavity. Since it was modified and popularized by Wichterman in 1980 [33], the CLP model has been considered the gold standard for sepsis research. Initially, CLP was not as widely used as lipopolysaccharide (LPS) as an inducer of DIC in animal models, probably because of its low reproducibility [34-36]. However, since its standardization by Rittirsch in PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/15556145 2009 [26], it has been possible to reproduce CLP exactly. Moreover, animals subjected to CLP simulate a true infectious septic state, and the decreased cardiovascular function and cardiac output induced by LPS are avoided [37]. In the CLP procedure used in the present study, the large ligation and needle size were necessary for high grade sepsis-induced DIC, and ensured 85 mortality at 72 h post-procedure. Dev.