Therefore, we speculated that it may be resulted from the increased activity of cholinergic receptors, the promoted release of Ach and the decreased expression of Ach. The underlying mechanism for the DCP improvement may be due to increases of cAMP in bladder, which could modulate the signaling pathways of neurotransmitter and receptors and increases of CGRP expression in bladder wall and DRG, leading to the enhancement of the contractility of the detrusor and sense of bladder filling. We have established a Rel report transgenic mouse model which can be used to monitor the endogenous Rel expression. Using in vivo bioluminescence imaging detection system, we demonstrated that luciferase activity in B6-Tg8Mlit mice was dramatically induced after i.p injection of LPS. The result of ex vivo experiment showed that the luciferase expression was induced in the heart, liver, spleen, lung, kidney, intestine, stomach, thymus and macrophages after the treatment with LPS, especially in the heart, liver, spleen, intestine and stomach. The data were in consistent with the change of endogenous murine Rel mRNA expression induced by LPS treatment. Meanwhile, the patterns of luciferase expression in LPS-treated B6-Tg8Mlit mice were also comparable to the results of Rel expression reported previously. The fold change did not match exactly between the luciferase activity and endogenous Rel mRNA expression. However, this is understandable that the protein level is often not in linear correlation with the endogenous mRNA expression in cells. Dexamethasone and aspirin, two well-known antiinflammatory drugs, suppressed the induction of luciferase expression and endogenous Rel expression in LPS treated B6-Tg8Mlit mice. These data demonstrate that the transgenic mice are faithful for monitoring Rel expression in vivo in c-Rel involved physiological or pathological processes and for evaluating the effects of anti-inflammatory drugs. LPS could induce Rel expression in monocytes and macrophages. We also collected macrophages from the abdomen fluid of the transgenic mouse. These specific cells manifested a good response of luciferase expression to LPS stimulus in vitro and could be used for high-throughput screening and studying of anti-inflammatory drugs at cellular level. Zymosan, a cell wall particle derived from Saccharomyces cerevisiae, is also widely used to induce inflammation in various relative experiments. However, the receptors for zymosan are distinct from those for LPS. LPS, the part of the outer cell wall of Gram negative bacteria, is detected by TLR4, while zymosan is recognized by TLR2 and TLR6. Although LPS and zymosan activates different triggers of target cells, the following inflammatory cascades seem to be similar. Our data also support the conclusion, for both LPS and zymosan could induce similar luciferase expression profiles in the B6-Tg8Mlit mice. The mouse EAE model is routinely used to study molecular mechanisms and signaling pathways of inflammatory regulation in Multiple sclerosis. It was reported that c-Rel-deficient mouse was resistant to the development of EAE due to its defective in the IL-12 and IFN-c induction and in the Th1 responses. It suggested that Rel expression was involved in the disease process of EAE. In our experiments, the luciferase expression in EAE group increased significantly at the eighth day after MOG injection before the loss of body weight and clinical symptoms occurred.

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