PDF(Pubmed)
Abstract：
Introduction: Asthma is a condition of airflow limitation, common throughout the world, with high mortality rates, especially as it still faces some obstacles in its management. As it constitutes a public health challenge, this study aimed to investigate the effect of copaiba oil (e.g., Copaifera langsdorffii), as a treatment resource, at doses of 50 and 100 mg/kg on certain mediators of acute lung inflammation (IL-33, GATA3, FOXP3, STAT3, and TBET) and early mechanisms of lung remodeling (degradation of elastic fiber tissues, collagen deposition, and goblet cell hyperplasia). Methods: Using an ovalbumin-induced acute allergic asthma model in BALB/c mice, we analyzed the inflammatory mediators through immunohistochemistry and the mechanisms of lung remodeling through histopathology, employing orcein, Masson\'s trichrome, and periodic acid-Schiff staining. Results: Copaiba oil treatment (CO) reduced IL-33 and increased FOXP3 by stimulating the FOXP3/GATA3 and FOXP3/STAT3 pathways. Additionally, it upregulated TBET, suggesting an additional role in controlling GATA3 activity. In the respiratory epithelium, CO decreased the fragmentation of elastic fibers while increasing the deposition of collagen fibers, favoring epithelial restructuring. Simultaneously, CO reduced goblet cell hyperplasia. Discussion: Although additional research is warranted, the demonstrated anti-inflammatory and re-epithelializing action makes CO a viable option in exploring new treatments for acute allergic asthma.
摘要：
简介：哮喘是气流受限的一种情况，全世界都很普遍，死亡率很高，特别是它在管理方面仍然面临一些障碍。因为它构成了公共卫生挑战，这项研究旨在调查Copaiba油的作用(例如，Copaiferalangsdorffii)，作为治疗资源，在50和100mg/kg的剂量下，对某些急性肺部炎症介质（IL-33，GATA3，FOXP3，STAT3和TBET）和肺重塑的早期机制（弹性纤维组织的降解，胶原蛋白沉积，和杯状细胞增生）。方法:采用卵清蛋白诱导的BALB/c小鼠急性过敏性哮喘模型,我们通过免疫组织化学分析了炎症介质，并通过组织病理学分析了肺重塑的机制，雇用orcein,马森的三色，和高碘酸希夫染色。结果：Copaiba油处理（CO）通过刺激FOXP3/GATA3和FOXP3/STAT3途径降低了IL-33并增加了FOXP3。此外,它上调了TBET，提示在控制GATA3活性方面的额外作用。在呼吸道上皮中，CO减少了弹性纤维的碎裂，同时增加了胶原纤维的沉积，有利于上皮重组。同时,CO减少杯状细胞增生。讨论：虽然有必要进行额外的研究，经证实的抗炎和再上皮化作用使CO成为探索急性过敏性哮喘新疗法的可行选择.
