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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/15497


    Title: Melatonin inhibits the formation of chemically induced experimental encapsulating peritoneal sclerosis through modulation of T cell differentiation by suppressing of NF-kappaB activation in dendritic cells
    Other Titles: Melatonin inhibits the formation of chemically induced experimental encapsulating peritoneal sclerosis through modulation of T cell differentiation by suppressing of NF-κB activation in dendritic cells
    Authors: Huang, SH;Hong, ZJ;Chen, MF;Tsai, MW;Chen, SJ;Cheng, CP;Sytwu, HK;Lin, GJ
    Contributors: National Institute of Infectious Diseases and Vaccinology
    Abstract: Encapsulating peritoneal sclerosis (EPS) is a severe complication of peritoneal dialysis (PD). Surgery is a therapeutic strategy for the treatment of complete intestinal obstruction. However, complete intestinal obstruction in long-term PD results in high mortality and morbidity rates after surgery. Immunopathogenesis participates in EPS formation: CD8, Th1, and Th17 cell numbers increased during the formation of EPS. The anti-inflammatory and immunomodulatory effects of melatonin may have beneficial effects on this EPS. In the present study, we determined that melatonin treatment significantly decreases the Th1 and Th17 cell populations in mice with EPS, decreases the production of IL-1β, TNF-α, IL-6, and IFN-γ, and increases the production of IL-10. The suppression of Th1 and Th17 cell differentiation by melatonin occurs through the inhibition of dendritic cell (DC) activation by affecting the initiation of the NF-κB signaling pathway in DCs. Our study suggests that melatonin has preventive potential against the formation of EPS in patients with PD.
    Date: 2023-11-27
    Relation: International Immunopharmacology. 2023 Nov 27;126:Article number 1111300.
    Link to: http://dx.doi.org/10.1016/j.intimp.2023.111300
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1567-5769&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:001129000000001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85178362261
    Appears in Collections:[司徒惠康] 期刊論文

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