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作 者:周艳[1,2] 阮征[1,2] 黄小流[1,2] 李玲[1,2] 刘文群[1,2] 温艳梅[1,2] 米书梅[1,2] 吴信[1,2,3] 印遇龙[1,2,3]
机构地区:[1]南昌大学食品科学与技术国家重点实验室,江西南昌330047 [2]南昌大学生命科学与食品工程学院,江西南昌330031 [3]中国科学院亚热带农业生态研究所,湖南长沙410125
出 处:《食品科学》2013年第17期236-240,共5页Food Science
基 金:国家自然科学青年科学基金项目(31001014);南昌大学食品科学与技术国家重点实验室青年骨干研究基金项目(SKLF-QN-201110)
摘 要:目的:以大鼠结肠炎作为肠道慢性炎症模型,观察低聚乳果糖(LS)对结肠炎大鼠血浆炎症水平及免疫细胞因子的影响,并探讨其改善大鼠肠道炎症可能的作用机制。方法:三硝基苯磺酸(TNBS)建立结肠炎大鼠模型,分为4组:正常组、模型组、LS组(灌胃250mg/(kg·d))、柳氮磺胺吡啶(SASP)药物组(灌胃250mg/(kg·d))。21d后宰杀大鼠,测定血浆碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)、诱生型一氧化氮合酶(iNOS)的活力,并测定IFN-γ、IL-4和IL-10的含量。结果:与正常组相比,TNBS造模后,血浆ALP的活力显著降低(P<0.01)以及IFN-γ的含量极显著升高(P<0.01)、IL-4的含量极显著降低(P<0.01),IL-10的含量显著降低(P<0.05),LDH和iNOS的活力以及IFN-γ/IL-4比值显著增高(P<0.05)。LS干预后,显著升高了血浆ALP的活力、IL-4和IL-10的含量,显著降低了iNOS的活力、IFN-γ/IL-4的比值。结论:LS能降低结肠炎大鼠血浆的炎症水平,其对结肠炎大鼠炎症的缓解可能是通过促进Th2型细胞因子的产生,调节Th1/Th2免疫平衡。Objective: To explore effect of lactosucrose (LS) on blood immunity and Th1/Th2 type cytokines in rats with colonitis. Methods: Experimental rat colitis was induced by trinitrobenzenesulfonic acid (TNBS) and randomly distributed into three groups as follows: model control (MC) group, LS group and SASP group. The normal control (NC) group was also included. All rats were killed on the 21st day. The activities of alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and inducible nitric oxide synthase (iNOS), and the contents of IFN-γ, IL-4 and IL-10, as well as IFN-γ/IL-4 ratio were measured in experimental colitis rats. Results: Compared with NC group, the activity of ALP and the content of IFN-γ were significantly increased (P 〈 0.01) and the content of IL-4 was significantly decreased (P 〈 0.01) in MC group. Moreover, the content of IL-10 was significantly decreased (P 〈 0.05), the activities of LDH and iNOS and IFN-γ/IL-4 ratio were significantly increased (P 〈 0.05). Compared with MC group, the activity of ALP and the contents of IL-4 and IL-10 in LS group were significantly increased, and the activity of iNOS and the ratio of IFN-γ/IL-4 were significantly decreased. Conclusion: The mechanism of LS in relieving inflammation in colitis may be achieved by increasing Th2 type cytokine production and rebalancing the Th1/Th2 immune response.
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