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巨噬细胞刺激蛋白和酪氨酸激酶受体RON在香烟诱导的大鼠气道炎症中的作用

Roles of macrophage stimulating protein and tyrosine kinase receptor RON in smoke-induced airway inflammation of rats.

作者信息

Wang Tao, Chen Xiaoju, Zhang Wenbo, Xiang Xiaojun, Leng Changyan, Jia Qinyao

机构信息

Department of Respiratory Medicine, Affiliated Hospital of North Sichuan Medical College Nanchong, Sichuan 637000, China.

出版信息

Int J Clin Exp Pathol. 2015 Aug 1;8(8):8797-808. eCollection 2015.

Abstract

OBJECTIVE

To investigate the roles of macrophage stimulating protein (MSP) and its tyrosine kinase receptor RON in smoke-induced airway inflammation of rats.

METHODS

Inhalation of combustion smoke was administered in rats to induce airway inflammation. Alveolar macrophages (AM) of healthy and smoking rats were isolated at different time points, cultured and then treated with different concentrations of MSP for 24 h.

RESULTS

When compared with healthy rats, MSP increased in the serum and bronchoalveolar lavage fluid (BALF) of smoking rats in a time dependent manner. In smoking rats, the RON expression in the lung and AM was higher than in healthy rats, and these increases were time dependent. MSP stimulated the production of malondialdehyde (MDA) and reduced superoxide dismutase (SOD) activity in rat AM cells in a dose dependent manner. MSP also stimulated the release of inflammatory factors TNF-α, IL-8, IL-1β and IL-10 in rat AM in a dose-dependent manner. Moreover, at the same MSP concentration, the contents of MDA, TNF-α, IL-8 and IL-1β in the AM of smoking rates were higher than in healthy rats, while the IL-10 content and SOD activity were lower than in healthy rats.

CONCLUSION

MSP and its receptor RON are involved in the smoke-induced airway inflammation in rats via promoting AM to release inflammatory cytokines and inducing the increase of oxygen free radical.

摘要

目的

探讨巨噬细胞刺激蛋白(MSP)及其酪氨酸激酶受体RON在烟雾诱导的大鼠气道炎症中的作用。

方法

对大鼠进行燃烧烟雾吸入以诱导气道炎症。在不同时间点分离健康大鼠和吸烟大鼠的肺泡巨噬细胞(AM),进行培养,然后用不同浓度的MSP处理24小时。

结果

与健康大鼠相比,吸烟大鼠血清和支气管肺泡灌洗液(BALF)中的MSP呈时间依赖性增加。在吸烟大鼠中,肺和AM中RON的表达高于健康大鼠,且这些增加呈时间依赖性。MSP以剂量依赖性方式刺激大鼠AM细胞中丙二醛(MDA)的产生并降低超氧化物歧化酶(SOD)活性。MSP还以剂量依赖性方式刺激大鼠AM中炎症因子TNF-α、IL-8、IL-1β和IL-10的释放。此外,在相同MSP浓度下,吸烟大鼠AM中MDA、TNF-α、IL-8和IL-1β的含量高于健康大鼠,而IL-10含量和SOD活性低于健康大鼠。

结论

MSP及其受体RON通过促进AM释放炎症细胞因子和诱导氧自由基增加参与烟雾诱导的大鼠气道炎症。

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