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作 者:刘丽娟[1] 王志斌[1] 王允亮[1] 许树青 魏仕兵[1] 李军祥[1]
机构地区:[1]北京中医药大学东方医院 [2]解放军61785部队门诊部
出 处:《北京中医药大学学报》2014年第10期691-695,I0003,共6页Journal of Beijing University of Traditional Chinese Medicine
基 金:北京中医药大学创新团队资助项目(No.2011-CXTD-24)
摘 要:目的研究青黛对溃疡性结肠炎(UC)体内、体外炎症模型的抗炎作用。方法大鼠随机分为正常组、模型组、青黛高剂量组、青黛低剂量组,以低浓度TNBS/乙醇溶液灌肠诱导大鼠实验性结肠炎体内炎症模型,连续以青黛高、低剂量混悬液灌胃治疗10 d,酶联免疫吸附法(ELISA)检测血清白细胞介素-1(IL-1)、IL-6、IL-8浓度。以脂多糖(LPS)刺激小鼠巨噬细胞株RAW264.7细胞24h诱导体外炎症模型,以MTT法检测青黛对细胞生存率的影响,以ELISA法研究青黛在直接干预、预防干预2种模式下对细胞培养液IL-6、肿瘤坏死因子-α(TNF-α)表达的影响。结果动物实验:模型组大鼠血清中IL-1、IL-6、IL-8浓度均明显高于空白组(P<0.05),青黛高剂量组血清中IL-1、IL-6、IL-8含量均明显低于模型组(P<0.05),青黛低剂量组血清IL-6、IL-8浓度明显低于模型组(P<0.05)。细胞实验:模型组中IL-6、TNF-α水平较正常组均有明显升高(P<0.05);青黛直接干预时,10μmol/L青黛组细胞培养液IL-6、TNF-α均较模型组有明显下降(P<0.05);青黛预防性干预时,10μmol/L青黛组IL-6明显下降(P<0.05)。结论青黛对溃疡性结肠炎有一定的体内、体外抗炎作用,抗炎机制可能为下调炎症因子的表达。Objective To study anti-inflammatory effect of Qingdai powder on rat model of ulcerative colitis(UC) and on murine macrophage RAW264.7 cells . Methods Overall SD rats were randomly divided into 4 groups: normal group, model group, Qingdai high-dose group (high-dose group) and Qingdai low-dose group(low-dose group). Rat model of UC was induced by intracolonical administration of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-ethanol solution. Qingdai suspension liquid was administered intragastrically once a day for 10 d. Serum concentration of IL-1 ,IL-6 and IL-8 was tested by ELISA assay. On the other hand, murine macrophage RAW264.7 cells were induced by 10~zg/mL LPS for 24 h to establish an UC inflammatory cell model. Cell viability was detected by MT-F assay to determine the safe range of concentrations. After direct and prophylactic intervention of high- , mid- and low-dose Qingdai suspension on RAW264. 7 eel1 respectively, concentration of IL-6 and TNF-ot in supernatant were tested by ELISA assay. Results Compared with normal group, serum concentration of IL-1 ,IL-6 and IL-8 in model group increased significantly (P 〈 0.05 ); compared with model group, those of IL-1, IL-6 and IL-8 in high-dose group, and IL-6 and IL-8 in low-dose group decreased significantly(P 〈 0.05). Compared with normal group, concentration of IL-6 and TNF-α in supernatant increased significantly in model group (P 〈 0.05). After direct intervention, those of IL-6 and TNF-α in supernatant in 10 μmol/L Qingdai group reduced significantly(P 〈 0.05) compared with model group; while after prophylactic intervention, only IL-6 in 10 μmol/L Qindai group reduced (P 〈 0. 05 ). Conclusion Effects of anti-inflammation of Qingdai showed both in vivo and in vitro, and the potential mechanism probably was through down-regulating the expression of inflammatory factors.
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