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咪唑斯汀对SP诱导小鼠皮肤产生LTB_4和IL-5的抑制作用观察 被引量:2

Inhibitory effects of mizolastine on substance P-induced production of leukotriene B_4 and interleukin 5 in mouse skin
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摘要 目的:观察咪唑斯汀(m izo lastine)对P物质(SP)诱导小鼠皮肤产生白三烯B4(LTB4)和白介素5(IL-5)的抑制作用。方法:小鼠接受不同浓度咪唑斯汀及对照药物灌胃,30 m in后在小鼠背部皮下注射SP,其后取注射部位皮肤制备组织匀浆,以竞争酶联免疫吸附(EL ISA)法检测LTB4和IL-5的表达水平。结果:咪唑斯汀预处理组小鼠皮肤组织匀浆的LTB4和IL-5水平较生理盐水对照组均有不同程度降低。10 m g/kg咪唑斯汀组小鼠皮肤中的LTB4和IL-5水平[(1.23±0.29)pg/m l和(34.28±11.00)pg/m l]与生理盐水对照组(5.52±1.88 pg/m l和179.62±46.25 pg/m l)及同剂量氯雷他定组[(3.89±1.27)pg/m l和(127.74±43.27)pg/m l]比较均有显著下降(P<0.05),而与3 m g/kg地塞米松组[(0.76±0.36)pg/m l和(23.82±11.11)pg/m l]比较则无显著性差异(P=0.161,P=0.508)。结论:咪唑斯汀能够剂量依赖性地抑制SP诱导的小鼠皮肤中LTB4和IL-5的产生,其抗瘙痒效应可能与其抗组胺抗炎的双重机制有关。 Objective: To observe the inhibitory effect of mizolastine on substance P(SP)-induced production of leukotriene B4(LTB4) and interleukin 5 (IL-5) in mouse skin. Methods: Mice were fed with different doses of mizolastine or other control drugs, 30 min after administration animals were injected intradermally with SP on the back. The treated skin samples were taken and competitive enzyme-link immunoassay (ELISA) method was applied to detect LTB4 and IL-5 in the skin samples. Results: The LTB4 and IL-5 levels in 10 mg/kg mizolastine group were (1.23±0. 29)pg/ml and (34.28±11.00)pg/ml, respectively, which were lower than those in saline control group [(5.52±1.88)pg/ml and (179.62±46.25)pg/ml respectively] or loratadine group [(3.89±1.27) pg/ml and (127.74±43.27) pg/ml respectively]. No significant difference was found between 10 mg/kg mizolastine group and dexamethasone group (P=0.161 and P=0.508). Conclusion: Mizolastine might inhibit the production of LTB4 and IL-5 induced by substance P in mouse skin, suggesting that anti-inflammatory effect and the blockade of histamine H1 receptors might be involved in its anti-pruritic mechanisms.
出处 《浙江大学学报(医学版)》 CAS CSCD 2006年第2期224-227,共4页 Journal of Zhejiang University(Medical Sciences)
关键词 苯咪唑类 咪唑斯汀 P物质 白三烯B4 白细胞介素5 Benzimidazoles Mizolastine Substance P Leukotriene B4 Interleukin-5
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参考文献12

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共引文献42

同被引文献15

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