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- 저자 : ( Xinyong Wan ) (검색결과 1 건)
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( Huatuo Zhu ),( Xinyong Wan ),( Wenguo Chen ),( Chaohui Yu ),( Min Yue ),( Yining Dai ),( Lihua Chen ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: It was recently reported that epigenetics might play an essential role in IBD. Bromo adjacent homology domain 1 (BAHD1), which involved in category of epigenetics maintains homeostasis by promoting heterochromatin formation. Our study aimed to investigate the underlying mechanism of BAHD1 in gut inflammation including IBD, seeking a new therapeutic target for the inflammation-associated colon disease. Methods: Experimental colitis was induced in C57BL/6 mice by dextran sulfate sodium administration. To simulate the intestinal inflammation microenvironment for epithelial cells, Caco-2 cells were exposed to a mixture of LPS, TNF-a, IL-1ß, and IFN-. BAHD1 expression was detected by quantitative PCR(qPCR), western blot and immunohistochemistry in both UC patients and mice model. Small interfering RNA was used to knock down BAHD1 level(siBAHD1) in Caco-2 cells and associated cytokines(CKs) expression were detected by either qPCR or ELISA. Possible mechanism involving in- flammatory pathways activation were addressed by western blot. Results: Murine model of UC-like inflammation was successfully established. And we found that BAHD1 existed in the normal internal crypt and surface epithelial cells ubiquitously. Compared with control group, BAHD1 expression in colon tissue were significantly decreased in both UC patients and mice model. In the vitro model system, we found that the protein level of BAHD1 was decreased in the stimulated Caco-2 cells. In addition, consistent with mRNA level of associated CKs enhanced in the siBAHD1 group within stimulatory factors, the interference group secreted more IL-6 and MCP-1 contents in the culture supernatant. As for potential mechanisms of BAHD1 in colitis, increased expression of TNFR1 was found in Caco-2 cells pre-treated with siBAHD1 in gut inflammation model, accompanying with the activation of IKK/ NF-κB and JNK/AP-1 pathways. Conclusions: Collectively, those findings provide evidence that BAHD1 might act as an indispensable safeguard to keep intestine immunological homeostasis.
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