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The purpose of this study was to screen the optimum extraction of polysaccharides (DOP) from Dendrobium officinale stem. Firstly, different methods, including hot water extraction (HWE), cold-pressing (CP), freeze-thawing cold-pressing (FTCP), ultrasonic-assisted hot water extraction (UHWE), microwave-assisted hot water extraction (MHWE) and enzyme-assisted hot water extraction (EHWE), were employed to extract DOP under their respective best parameters. Then, the extraction yield, structure and antioxidant activity of the polysaccharides from different extraction methods were compared under the same condition. The data implied that UHWE and FTCP possessed higher extraction yield than the other extraction methods. Besides, DOPCP and DOPFTCP had higher molecular weight than the other polysaccharide samples. More importantly, DOPFTCP had the highest antioxidant activity. Overall, DOPFTCP exhibit high extraction yield, well-preserved molecular chains and best antioxidant activity, all these indicated FTCP was the most suitable method to extract DOP.

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 β-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 β-arrestin1 signaling pathways.