论文部分内容阅读
目的探究吴茱萸碱(evodiamine,EVO)对酵母多糖(zymosan)诱导的急性肺损伤的保护效应及其作用机制。方法 24只6~8周龄雄性C57BL/6小鼠,按随机数字表法分为正常对照组、EVO对照组、模型组、EVO治疗组,每组6只。各组分别于处理作用12 h后处死小鼠,收集眼眶血及肺组织。酶联免疫吸附法(ELISA)检测血液及肺组织中白介素-6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)水平及肺组织髓过氧化物酶(myeloperoxidase,MPO)活性及核转录因子NF-κB p65的DNA结合活性,TUNEL法检测肺组织细胞凋亡情况,HE染色观察肺组织病理改变并测量肺湿干质量比。结果酵母多糖作用12 h后,小鼠出现精神萎靡、活动减少等症状。EVO治疗组小鼠状态有所好转。EVO可明显改善酵母多糖所致的肺泡壁毛细血管扩张充血及炎性细胞浸润,降低肺湿干质量比,并显著下调酵母多糖刺激下血清和肺脏中IL-6和TNF-α的含量(P<0.01),同时抑制肺组织中MPO含量以及NF-κB p65的DNA结合活性(P<0.01)。结论 EVO可缓解酵母多糖诱导的急性肺损伤。该作用可能是通过抑制NF-κB的活性以减少炎症介质释放实现。
Objective To investigate the protective effect of evodiamine (EVO) on acute lung injury induced by zymosan and its mechanism. Methods Twenty-four male C57BL / 6 mice aged 6-8 weeks were divided into normal control group, EVO control group, model group and EVO treatment group by random number table. The mice were sacrificed 12 h after treatment, respectively, and orbital blood and lung tissue were collected. The level of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and the level of myeloperoxidase in lung and blood were detected by enzyme linked immunosorbent assay (ELISA) The activity of myeloperoxidase (MPO) and the DNA binding activity of NF-κB p65 were detected. TUNEL method was used to detect the apoptosis of lung tissue. The pathological changes of lung tissue were observed by HE staining and the lung wet mass ratio was measured. Results After 12 hours of action of zymosan, the mice showed apathetic symptoms and decreased activities. EVO treatment group mouse state has improved. EVO can significantly improve the alveolar wall telangiectasia and inflammatory cell infiltration caused by zymosan, reduce the mass ratio of lung wet to dry, and significantly downregulate the levels of IL-6 and TNF-α in serum and lungs stimulated by zymosan (P <0.01), while inhibiting MPO content in lung tissue and DNA binding activity of NF-κB p65 (P <0.01). Conclusion EVO can relieve the acute lung injury induced by zymosan. This effect may be through the inhibition of NF-κB activity to reduce the release of inflammatory mediators.