Abstract：
BACKGROUND: Pulmonary fibrosis (PF) is a chronic, progressive, and irreversible heterogeneous disease of lung interstitial tissue. To combat progression of PF, new drugs are required to be developed. Rhizoma coptidis (COP), one of the main alkaloids of Coptis chinensis, is a traditional herbal medicine used to treat various inflammatory diseases.
OBJECTIVE: To investigate the possible effects of Coptisine (Cop) on the growth, inflammation, as well as FMT of TNF-β1-induced HFL1 cells and uncover the mechanism.
METHODS: Human fetal lung fibroblast 1 (HFL1) was induced using 6ng/mL TGF-β1 as a model of pulmonary fibrosis. CCK-8, Brdu, and transwell assays indicated the effects on cell growth as well as motility. qPCR and the corresponding kits indicted the effects on cell inflammation. Immunoblot showed the effects on FMT and further confirmed the mechanism.
RESULTS: Coptisine inhibits excessive growth as well as motility of TNF-β1-induced HFL1 cells. It further inhibits inflammation and ROS levels in TNF-β1-induced HFL1 cells. Coptisine inhibits the FMT process of TNF-β1-induced HFL1 cells. Mechanically, coptisine promotes the Nrf2/HO-1 pathway.
CONCLUSIONS: Coptisine can inhibit the excessive growth, inflammation as well as FMT of lung fibroblasts into myofibroblasts. It could serve as a promising drug of PF.
OBJECTIVE: To investigate the possible effects of Coptisine (Cop) on the growth, inflammation, as well as FMT of TNF-β1-induced HFL1 cells and uncover the mechanism.
METHODS: Human fetal lung fibroblast 1 (HFL1) was induced using 6ng/mL TGF-β1 as a model of pulmonary fibrosis. CCK-8, Brdu, and transwell assays indicated the effects on cell growth as well as motility. qPCR and the corresponding kits indicted the effects on cell inflammation. Immunoblot showed the effects on FMT and further confirmed the mechanism.
RESULTS: Coptisine inhibits excessive growth as well as motility of TNF-β1-induced HFL1 cells. It further inhibits inflammation and ROS levels in TNF-β1-induced HFL1 cells. Coptisine inhibits the FMT process of TNF-β1-induced HFL1 cells. Mechanically, coptisine promotes the Nrf2/HO-1 pathway.
CONCLUSIONS: Coptisine can inhibit the excessive growth, inflammation as well as FMT of lung fibroblasts into myofibroblasts. It could serve as a promising drug of PF.
摘要：
背景：肺纤维化（PF）是一种慢性，进步,和不可逆的肺间质组织异质性疾病。为了对抗PF的发展，需要开发新药物。黄连(COP),黄连的主要生物碱之一，是一种用于治疗各种炎症性疾病的传统草药。
目的：为了研究黄连碱（Cop）对生长的可能影响，炎症,以及TNF-β1诱导的HFL1细胞的FMT，并揭示其机制。
方法：使用6ng/mLTGF-β1诱导人胎儿肺成纤维细胞1（HFL1）作为肺纤维化模型。CCK-8,Brdu,和transwell测定表明对细胞生长和运动的影响。qPCR和相应的试剂盒指示了对细胞炎症的影响。免疫印迹显示了对FMT的影响，并进一步证实了其机制。
结果：黄连碱抑制TNF-β1诱导的HFL1细胞的过度生长和运动。它进一步抑制TNF-β1诱导的HFL1细胞中的炎症和ROS水平。黄连碱抑制TNF-β1诱导的HFL1细胞的FMT过程。机械上,黄连碱促进Nrf2/HO-1通路。
结论：黄连碱可以抑制小鼠的过度生长，炎症以及肺成纤维细胞转化为肌成纤维细胞的FMT。它可以作为PF的一种有前途的药物。
目的：为了研究黄连碱（Cop）对生长的可能影响，炎症,以及TNF-β1诱导的HFL1细胞的FMT，并揭示其机制。
方法：使用6ng/mLTGF-β1诱导人胎儿肺成纤维细胞1（HFL1）作为肺纤维化模型。CCK-8,Brdu,和transwell测定表明对细胞生长和运动的影响。qPCR和相应的试剂盒指示了对细胞炎症的影响。免疫印迹显示了对FMT的影响，并进一步证实了其机制。
结果：黄连碱抑制TNF-β1诱导的HFL1细胞的过度生长和运动。它进一步抑制TNF-β1诱导的HFL1细胞中的炎症和ROS水平。黄连碱抑制TNF-β1诱导的HFL1细胞的FMT过程。机械上,黄连碱促进Nrf2/HO-1通路。
结论：黄连碱可以抑制小鼠的过度生长，炎症以及肺成纤维细胞转化为肌成纤维细胞的FMT。它可以作为PF的一种有前途的药物。
