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作 者:苏韦 陈鸿鹏 SU Wei;CHEN Hongpeng(School of Traditional Chinese Medicine,Guangdong Pharmaceutical University,Guangzhou,Guangdong 510006,China)
出 处:《食品与机械》2024年第6期158-163,共6页Food and Machinery
基 金:云浮市科技局项目(编号:2022020407);广东省卫生健康委员会项目(编号:B2023233);广东省科技厅项目(编号:KTP20200175)。
摘 要:[目的]探究山药多糖(YP)对溃疡性结肠炎(UC)小鼠的改善作用。[方法]设空白组、YP组、DSS组和DSS+YP组。通过饮用DSS水溶液搭建模型,治疗组连续灌胃给药7 d。检测各小鼠体重、疾病活动指数(DAI)评分、结肠中炎症因子和NLRP3炎症小体含量,并进行HE染色分析。用含1μg/mL脂多糖(LPS)的培养液处理RAW 264.7巨噬细胞24 h建立体外细胞炎症模型,同时将一定浓度的YP溶液加入到培养液中与LPS共孵育24 h,酶联免疫吸附试验法检测细胞培养上清中IL-1β、IL-6和TNF-α的含量;免疫印迹法分析细胞中NLRP3炎症小体相关蛋白的表达水平。[结果]与空白组相比,DSS组小鼠体重下降,染色展现大区域溃疡,DAI和炎症因子含量升高。与DSS组相比,DSS+YP组小鼠的肠道损伤得到显著改善,肠道组织中IL-1β、IL-6、TNF-α表达和NLRP3炎症小体激活信号均被显著抑制。在细胞炎症模型中,YP干预处理可显著抑制LPS所致的IL-1β、IL-6和TNF-α的分泌和NLRP3蛋白的表达。[结论]YP可改善DSS引起的小鼠UC,其机制是阻碍NLRP3炎症小体的激活来实现。[Objective]This study aimed to investigate the effects of Yam Polysaccharide(YP)on ulcerative colitis(UC)mice.[Methods]The study included a blank group,YP group,DSS group,and DSS+YP group.The UC model was established by administering DSS water solution,and the treatment group received oral administration of YP for 7 days.Measurement of body weight,DAI score,inflammatory factors in the colon,NLRP3 inflammasome,and HE staining were conducted to evaluate the effects.RAW 264.7 macrophages were treated with 1μg/mL lipopolysaccharide(LPS)for 24 h to establish the cell inflammation model in vitro.A certain concentration of YP solution was added to the culture medium and incubated with LPS for 24 h.The contents of IL-1β,IL-6 and TNF-αin the cell culture supernatance were detected by enzyme-linked immunosorbent assay.The expression level of NLRP3 inflammator-related protein was analyzed by Western blotting.[Results]Compared to the blank group,the DSS group showed weight loss,extensive ulceration in staining,increased DAI score,and elevated levels of inflammatory factors.Compared to the DSS group,the DSS+YP group showed significant improvement in intestinal damage,and the expression of IL-1β,IL-6,TNF-α,and activation of NLRP3 inflammasome signaling were significantly inhibited in intestinal tissues.In the cell inflammation model,YP pretreatment significantly suppressed the secretion of IL-1β,IL-6,TNF-αinduced by LPS,as well as the expression of NLRP3 protein.[Conclusion]YP can improve DSS-induced UC in mice by inhibiting the activation of NLRP3 inflammasome.
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