Mao Mingqing, Li Jing, Bi Aiping, Jia Hui, Li Qiong, Liu Yang, Jiang Xiaochuan, Huang Desheng, Xia Shuyue
Department of Respiratory and Critical Care Medicine, Central Hospital Affiliated to Shenyang Medical College, Shenyang, People's Republic of China.
Shenyang Environment Monitor Central Station, Key Laboratory of Atmospheric Organic Compound Monitoring and Analysis, Ministry of Environmental Protection, Shenyang, People's Republic of China.
Exp Lung Res. 2020 Oct;46(8):297-307. doi: 10.1080/01902148.2020.1801895. Epub 2020 Aug 4.
This study aims to explore the effect of thymoquinone (TQ) on particulate matter 2.5 (PM2.5)-induced lung injury.
The PM2.5 sample was provided by Shenyang Environment Monitor Central Station. Lung injury was established by intratracheal instillation PM2.5 (7.5 mg/kg) followed by TQ treatment (20 and 40 mg/kg) for 14 d in rats. Hematoxylin and eosin (HE) and Evans blue dye (EBD) staining were detected on lung tissues. ELISA, real-time PCR, western blotting and TUNEL assays were also performed.
The data showed that TQ diminished lung injury and EBD accumulation. The number of macrophages, neutrophils, eosinophils, and lymphocytes was ameliorated after TQ treatment. In addition, TQ suppressed the inflammation reaction parameters (interleukin-1β and -6, IL-1β and IL-6; tumor necrosis factor-α, TNF-α) and oxidative stress in PM2.5-induced lung injury. The levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase (HO-1) were increased due to the treatment of TQ. The number of TUNEL-positive cells was prominently reduced in TQ-treated rats compared with that in PM2.5 group. Intratracheal instillation PM2.5 activated autophagy, whilst TQ blocked it in lung.
Taken together, this study provides the first evidence that TQ suppresses inflammation, oxidative stress, apoptosis, and autophagy in PM2.5-induced lung injury.
本研究旨在探讨百里醌(TQ)对细颗粒物2.5(PM2.5)所致肺损伤的影响。
PM2.5样本由沈阳市环境监测中心站提供。通过气管内滴注PM2.5(7.5mg/kg)建立大鼠肺损伤模型,随后用TQ(20和40mg/kg)治疗14天。对肺组织进行苏木精-伊红(HE)染色和伊文思蓝染料(EBD)染色检测。还进行了酶联免疫吸附测定(ELISA)、实时聚合酶链反应(real-time PCR)、蛋白质印迹法(western blotting)和末端脱氧核苷酸转移酶介导的缺口末端标记(TUNEL)检测。
数据显示,TQ减轻了肺损伤和EBD蓄积。TQ治疗后,巨噬细胞、中性粒细胞、嗜酸性粒细胞和淋巴细胞数量得到改善。此外,TQ抑制了PM2.5所致肺损伤中的炎症反应参数(白细胞介素-1β和-6,IL-1β和IL-6;肿瘤坏死因子-α,TNF-α)和氧化应激。由于TQ的治疗,核因子红细胞2相关因子2(Nrf2)和血红素加氧酶(HO-1)水平升高。与PM2.5组相比,TQ治疗组大鼠的TUNEL阳性细胞数量显著减少。气管内滴注PM2.5激活了自噬,而TQ在肺中阻断了自噬。
综上所述,本研究首次提供证据表明,TQ可抑制PM2.5所致肺损伤中的炎症、氧化应激凋亡和自噬。