孟鲁司特对过敏性紫癜小鼠炎性因子的影响及其作用机制 |
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引用本文: | 杨云,马喜兴,王大虎,张环环,马耀辉,任翠敏,刘强.孟鲁司特对过敏性紫癜小鼠炎性因子的影响及其作用机制[J].中国免疫学杂志,2018,34(8):1222. |
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作者姓名: | 杨云 马喜兴 王大虎 张环环 马耀辉 任翠敏 刘强 |
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作者单位: | 河北医科大学第二医院皮肤科 |
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摘 要: | 目的:探讨孟鲁司特对过敏性紫癜小鼠炎性因子的影响及其作用机制。方法:采用灌胃给予0.1% 麦胶蛋白
(溶于6 mmol/ L HCl 酸化水),尾静脉注射印度墨水(40 mg/ kg)封闭网状内皮系统的方法建立过敏性紫癜小鼠模型,采用印度
墨水小鼠碳粒廓清法检测网状内皮系统(RES)功能,采用微量聚乙二醇沉淀法测定血清循环免疫复合物(CIC)含量,采用分
光光度法测定晚期氧化蛋白产物(AOPPs),采用酶联免疫吸附实验测定IL-1β、IL-6、TNF-α含量。结果:与空白组比较,模型
组小鼠RES 功能显著降低,血清CIC、AOPPs、IL-1β、IL-6、TNF-α的水平显著升高(P<0.05);与模型组比较,低、中、高浓度孟
鲁司特组小鼠RES 功能显著提高,血清CIC、AOPPs、IL-1β、IL-6、TNF-α的水平显著降低(P<0.05)。结论:孟鲁司特可以减轻
过敏性紫癜小鼠症状,其作用机制与降低氧化应激反应、降低血清AOPPs 的含量水平、抑制炎症反应、提高RES 功能和增强循
环免疫复合物的消除能力有关。
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关 键 词: | 过敏性紫癜 孟鲁司特 炎性因子 晚期氧化蛋白产物 |
Effect and mechanism of montelukast on inflammatory cytokines in Henoch-#br# Schonlein purpura mice |
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Abstract: | Objective:To investigate the effect and mechanism of montelukast on inflammatory cytokines in Henoch-Schonlein
purpura model mice.Methods:Henoch-Schonlein purpura model mice were built by 0.1% Gliadin(Dissolved in 6 mmol/ L HCl,ig) as
antigen and India ink(40 mg/ kg,ip) to close reticuloendothelial system.The function of reticuloendothelial system was detected by
Indian ink mice carbon clearance.Trace polyethylene glycol precipitation was used to determine the content of the circulating immune
complex(CIC) in serum.Spectrophotometry was used to determine the content of advanced oxidation protein products(AOPPs).
Enzyme-linked immunosorbent assay was used to determine the content of IL-1β,IL-6 and TNF-α.Results:Compared with control
group,CIC,AOPPs,IL-1α,IL-6 and TNF-αin serum of the mice in model group were significantly increased while the function of RES
was significantly reduced(P<0.05).Compared with model group,CIC,AOPPs,IL-1β,IL-6 and TNF-αin serum of the mice in different
dose group were significantly reduced while the function of RES was significantly increase(P<0.01).Conclusion:Montelukast can
alleviate the symptom of Henoch-Schonlein purpura mice by reducing oxidative stress response,reducing AOPPs levels in serum,
inhibiting inflammatory reaction,improving the function of RES,enhancing the ability to eliminate cyclic immune complexes. |
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