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作 者:曹雯[1] 刘欢[2] 韩清娟[2] 管潇 冯志强 曹文轩 秦建波 李滨 张梦军[1] 张惠静[1]
机构地区:[1]第三军医大学药学院药物分析与分析化学教研室,重庆400038 [2]第三军医大学药学院化学教研室,重庆400038 [3]重庆市科学技术研究院,401123
出 处:《免疫学杂志》2015年第1期12-16,共5页Immunological Journal
基 金:重庆市基础与前沿研究计划(cstc2013jcyj A10098)
摘 要:目的研究(E)-苯乙基-3-(3,5-二羟基-4-异丙基苯基)丙烯酸酯(THCA354)化合物的抗炎作用及抗炎初步机制。方法通过二甲苯和佛波酯诱导的小鼠耳肿胀模型来评价THCA354的抗炎作用;进一步通过佛波酯诱导的小鼠耳肿胀模型来评价该化合物对小鼠耳组织中髓过氧化酶(MPO)的活性和IL-1β、IL-6、TNF-α炎症细胞因子的抑制作用。结果与模型组相比,局部涂抹THCA354化合物的小鼠耳朵厚度,淋巴细胞的浸润,耳组织中髓过氧化物酶活性和IL-1β、IL-6、TNF-α炎症细胞因子的表达均显著降低。结论 THCA354化合物可能通过抑制中性粒细胞的活化和IL-1β、IL-6、TNF-α炎症细胞因子的释放从而有效地缓解小鼠耳组织炎症水肿和淋巴细胞的浸润,发挥抗炎作用。The present study was designed to investigate the anti-inflammatory effects of(E)-phenenthyl-3-(3,5-dihydroxy-4-isopropyl phenyl) acrylate compound(THCA354) and explored its tentative mechanisms. We evaluated the anti-inflammatory effect of THCA354 on 12-O-tetradecanoylphorbol-13-acetate(TPA) or xylene induced ear edema in mice in vivo, while the anti-inflammatory mechanism was explored by determining the activity of myeloperoxidase(MPO) and protein levels of inducible tumor necrosis factor-α(TNF-α), interleukin(IL)-1β, and IL-6 on TPA induced ear edema model. Data showed that topical treatment with THCA354 compound leading to substantial reductions in skin thickness and cells infiltration, neutrophil-mediated myeloperoxidase activity, and various histopathological indicators. The THCA354 compound treatment also significantly reduced the protein levels of TNF-α, IL-6 and IL-1β at the application sites in mouse model of inflammation induced by TPA.These results indicated that THCA354 has anti-inflammatory activities that may be mediated, at least in part, by blocking the neutrophil-mediated myeloperoxidase activity and protein levels of a panel of inflammatory mediators including TNF-α, IL-1β, and IL-6.
关 键 词:多酚类化合物 抗炎作用 TPA诱导的小鼠耳肿胀模型 二甲苯诱导的小鼠耳肿胀模型
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