4.7 Article

Therapeutic roles of polysaccharides from Dendrobium Officinaleon colitis and its underlying mechanisms

期刊

CARBOHYDRATE POLYMERS
卷 185, 期 -, 页码 159-168

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.carbpol.2018.01.013

关键词

Polysaccharides; Dendrobium officinale; Ulcerative colitis; NLRP3 inflammasome; beta-Arrestin1

资金

  1. Guangdong Province Universities and Colleges the Special Funds from Central Finance of China in Support of the Development of Local Colleges and University [A1-AFD018171Z11026, A1-AFD01515A03, A1-AFD016151Z3207]
  2. Science and Technology Project Scheme of Guangdong Province [2013A022100002, 2015A030313044]
  3. Hong Kong, Macao and Taiwan Special Science and Technology Cooperation Program [2014DFH30010]
  4. Pearl-River Scholar Funded Scheme
  5. Six Talent Peaks Project in Jiangsu Province [2017-YY-003]
  6. Qing Lan Project of Jiangsu Province
  7. Open fund of Jiangsu Provincial Key Laboratory of Palygorskite Science and Applied Technology [HPK201704]

向作者/读者索取更多资源

Polysaccharide, as a promising candidate to meet the medication requirement of ulcerative colitis (UC), is increasingly attracting extensive interest. Dendrobium officinale has been widely used to treat gastrointestinal sickness in the clinical treatment of Traditional Chinese Medicine. However, it remains largely unknown whether polysaccharides (DOPS) from Dendrobium officinale can treat UC. The purpose of this paper is to confirm therapeutic action of DOPS to UC and explored its underlying mechanisms. We noted that DOPS could dramatically improve clinical signs and symptoms, decrease mortality, alleviate colonic pathological damage, and reestablish the balance of pro-and anti-inflammatory cytokines in DSS-induced acute UC mice. Moreover, DOPS treatment could also markedly suppress the activation of NLRP3 inflammasome and beta-arrestin1 in vivo and in vitro. This study showed that DOPS possesses appreciable therapeutic effect to treat experimental acute UC mice. Its mechanism could be related to inhibition of NLRP3 inflammasome and beta-arrestin1 signaling pathways.

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