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Fibroblast growth factor 10 alleviates particulate matter-induced lung injury by inhibiting the HMGB1-TLR4 pathway

机译:成纤维细胞生长因子10通过抑制HMGB1-TLR4途径减轻颗粒物诱导的肺损伤

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摘要

Exposure to particulate matter (PM) is associated with increased incidence of respiratory diseases. The present study aimed to investigate the roles of fibroblast growth factor 10 (FGF10) in PM-induced lung injury. Mice were intratracheally instilled with FGF10 or phosphate-buffered saline at one hour before instillation of PM for two consecutive days. In addition, the anti-inflammatory impact of FGF10 and its effect on the high-mobility group box 1 (HMGB1)-toll-like receptor 4 (TLR4) pathway was investigated. It was found that PM exposure is associated with increased inflammatory cell infiltration into the lung and increased vascular protein leakage, while FGF10 pretreatment attenuated both of these effects. FGF10 also decreased the PM-induced expression of interleukin (IL)-6, IL-8, tumor necrosis factor-α and HMGB1 in murine bronchoalveolar lavage fluid and in the supernatants of human bronchial epithelial cells exposed to PM. FGF10 exerted anti-inflammatory and cytoprotective effects by inhibiting the HMGB1-TLR4 pathway. These results indicate that FGF10 may have therapeutic values for PM-induced lung injury.
机译:接触颗粒物(PM)与呼吸系统疾病的发生率增加相关。本研究旨在调查成纤维细胞生长因子10(FGF10)在PM诱导的肺损伤中的作用。在连续两天滴入PM之前的一小时,向小鼠气管内滴入FGF10或磷酸盐缓冲盐水。此外,研究了FGF10的抗炎作用及其对高迁移率族框1(HMGB1)-toll样受体4(TLR4)途径的影响。发现PM暴露与炎性细胞向肺部浸润增加和血管蛋白泄漏增加有关,而FGF10预处理减弱了这两种作用。 FGF10还降低了PM诱导的鼠肺支气管灌洗液和暴露于PM的人支气管上皮细胞上清液中白介素(IL)-6,IL-8,肿瘤坏死因子-α和HMGB1的表达。 FGF10通过抑制HMGB1-TLR4途径发挥抗炎和细胞保护作用。这些结果表明FGF10对于PM诱导的肺损伤可能具有治疗价值。

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