Objective:To investigate the potential role of NF-kB inflammatory signaling pathways in macrophages over-activation during systemic inflammatory responses syndrome, and also to observe NF-KBp65/p50 activation and nuclear translocation, IKK activation, expressions of inflammatory cytokines; then expound the coordinated regulatory responses of IKK a & y on multiple taches of the above signaling pathway, and the mechanisms about emodin's treating effects; thus furtherly present the double-function of Nitric oxide on acute lung injury induced by severe acute pancreatitis, and the relationship with NF-kB activation, aimed to provide experimental evidences for treating systemic inflammatory responses diseases and looking for more fitable drug-effecting targets.Methods:Part one: It was thus aimed to investigate the regulatory mechanism of emodin on LPS-induced inflammatory responses in RAW264.7 macrophages by the methods of RT-PCR, Western Blot analysis, immunocytochemical staining (ICC) and immunofluorescence (IF) analysis. The experiments were composed of 7 groups with 5 dishes per group. Group 1: RAW264.7 cells in normal culture; Group 2, 3, and 4: the cells cultured in the medium containing LPS (10μg/ml) at 30 min, 2 hours, 5 hours,...
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