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百草枯中毒致大鼠肺纤维化模型中肺组织的IL-17A表达 被引量:3

The increased expression of IL-17A in lung tissue of Paraquat-induced rat pulmonary fibrosis model
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摘要 目的观察百草枯中毒大鼠血浆和肺组织匀浆中的IL-17A的动态变化,探讨大鼠百草枯中毒肺损伤的机制。方法将雄性SD大鼠24只随机分成百草枯中毒模型组和生理盐水对照组,分别给予20 mg/kg百草枯或等体积生理盐水1次性灌胃染毒,并在给药后7 d和14 d处死大鼠,观察其肺的病理变化。肺组织匀浆和血浆中IL-17A的含量。结果百草枯中毒后大鼠肺部病理切片表现为肺泡炎,肺纤维化等不同程度的肺损伤改变。血浆和组织匀浆中IL-17A在中毒后与对照组大鼠比较明显升高,并随时间变化,比较差异有统计学意义(P<0.05)。结论在百草枯中毒肺损伤中,IL-17A可能发挥了重要作用。 Objective To observe the change of IL-17A in paraquat (PQ) poisoning rats and to explore the mechanism of lung injury caused by PQ poisoning. Methods 24 Male SD rats were randomly assigned to PQ poisoning group and control group. Rats in the PQ group were each given a single intraperitoneal injection of PQ (20mg/kg body weight), while normal saline was injected to the rats in the control group. The rats were sacrificed at 7 days and 14 days after the administration of PQ. The pathological changes of the lung were studied.IL- 17A levels in lung homogenates and in blood were measured. Results Inflammatory cell infiltration and fibrotic scores were more prominent in the model group compared to the control group. IL-17A levels in the lung homogenate and blood of PQ group were significantly higher than those in the control group (P〈0.05). Conclusion IL-17A may play an important role in paraquat-induced lung damage.
机构地区 安徽省立医院ICU
出处 《湖南中医药大学学报》 CAS 2012年第12期15-16,共2页 Journal of Hunan University of Chinese Medicine
基金 安徽高校省级自然科学研究项目(NO:KJ2011Z203)
关键词 IL-17A 百草枯 中毒 大鼠肺纤维化 IL-17A Paraquat Poisoning
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  • 1Boniface K,Blom B,Liu YJ,et al.de Waal Malefyt R.From interleukin-23 to T-helper 17 cells:human T-helper cell differentiation revisited[J].Immunol Rev,2008,22(6): 132-146.
  • 2Szapiel SV, Elson NA,Fulmer JD,et al.Bleomycin-induced interstitial pulmonary disease in the nude athymic mouse[J].Am Rev Respir Dis, 1979,120(4):893-899.
  • 3Chen CM,Lua AC.Lung toxicity of paraquat in the rat[J].J Toxicol Environ Health A,2000,60(7):477-487.
  • 4Dinis-Oliveira RJ,Duarte JA,Sanchez-Navarro A,et al.Paraquat poisonings: mechanisms of lung toxicity clinical features and treatment [J]. Crit Rev Toxicol,2008,38 ( 1 ): 13 -71.

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