摘要
目的研究成纤维细胞生长因子-21(fibroblast growth factor-21,FGF-21)抑制脂多糖(LPS)诱导的急性炎症的作用及机制。方法构建LPS诱导的小鼠急性炎症模型,FGF-21高、中、低剂量进行处理后,HE染色法观察肺部组织病理学变化,ELISA法检测血清中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β、IL-6、IL-17含量,实时荧光定量聚合酶链反应(PCR)法检测TNF-α、IL-1β、IL-6、IL-17表达量,激光共聚焦和Western blot法检测腹腔巨噬细胞核因子(NF)-κB蛋白向细胞核内转移情况。结果 FGF-21干预后,模型小鼠肺部损伤明显减轻,炎性浸润细胞减少。血清和腹腔巨噬细胞中TNF-α、IL-1β、IL-6、IL-17含量均显著降低且成剂量依赖性趋势。激光共聚焦和Western-blot结果均显示,FGF-21能够抑制NF-κB向细胞核内转移。结论 FGF-21能够作用于巨噬细胞调控机体免疫系统,通过NF-κB信号通路缓解小鼠炎症反应状态可能是FGF-21调节免疫系统的机制之一。
OBJECTIVE To study the effects of fibroblast growth factor-21 （FGF-21） on acute inflammation induced by lipopo- lysaccharide （LPS） and its mechanism. METHODS Mouse model of acute inflammation was established by injection of LPS and treated with FGF-21 at high, medium and low doses, the pathological changes were detected with HE staining, the expression level of TNF-α, IL-1β, IL-6 and IL-17 in serum and peritoneal macrophage were determined by ELISA and Real-time PCR. NF-KB p65 in macrophage cells was analyzed by confocal laser scanning microscope and Western-blotting. RESULTS FGF-21 treatment reduced lung damage and inflammatory cell infiltration and decreased the expression level of TNF-α, IL-113, IL-6 and IL-17 in both serum and peritoneal macrophage. The results of confocal laser scanning microscope and Western-blotting both showed that FGF-21 could inhibit NF-kB transferring to the nucleus. CONCLUSION FGF-21 could regulate the imnmne system by acting on macrophage. Relieving the inflammatory response in mice through NF-kB signal pathway may be one of the mechanisms FGF-21 regulating immune system.
出处
《中国药学杂志》
CAS
CSCD
北大核心
2016年第15期1282-1288,共7页
Chinese Pharmaceutical Journal
基金
黑龙江省应用技术研究与开发计划资助项目(GC14D205)
哈尔滨商业大学博士科研启动项目(92508177)
