肺纤维化是一种异质性肺病，其特点是瘢痕组织过度积累，导致肺结构破坏和通气受限。本研究旨在检验肉桂酸对甲氨蝶呤引起的肺纤维化可能的保护作用。大鼠口服给予肉桂酸（50mg/kg/天）预处理14天，实验的第5天和第12天口服给予甲氨蝶呤（14mg/kg）。吡非尼酮（50mg/kg/天）作为标准药物。实验结束时，测量了肺组织的氧化参数（丙二醛，粒细胞过氧化物酶，一氧化氮，和总谷胱甘肽）和炎症介质（肿瘤坏死因子-α和白细胞介素-8），以及转化生长因子-β和胶原含量作为纤维化指标。结果表明，肉桂酸如同吡非尼酮一样有效地防止了甲氨蝶呤引起的明显病理损伤。这与氧化、炎症和纤维化参数的改善相平行。肉桂酸治疗的结果与吡非尼酮相差不大。总之，肉桂酸的预处理可以保护机体免受甲氨蝶呤引起的纤维化，使其成为潜在的甲氨蝶呤辅助预防治疗，可预防其可能诱导肺纤维化的作用。© 2023. 作者。

Lung fibrosis is a heterogeneous lung condition characterized by excessive accumulation of scarred tissue, leading to lung architecture destruction and restricted ventilation. The current work was conducted to examine the probable shielding influence of cinnamic acid against lung fibrosis induced by methotrexate.Rats were pre-treated with oral administration of cinnamic acid (50 mg/kg/day) for 14 days, whereas methotrexate (14 mg/kg) was orally given on the 5th and 12th days of the experiment. Pirfenidone (50 mg/kg/day) was used as a standard drug. At the end of the experiment, oxidative parameters (malondialdehyde, myeloperoxidase, nitric oxide, and total glutathione) and inflammatory mediators (tumor necrosis factor-α and interleukin-8), as well as transforming growth factor-β and collagen content, as fibrosis indicators, were measured in lung tissue.Our results revealed that cinnamic acid, as pirfenidone, effectively prevented the methotrexate-induced overt histopathological damage. This was associated with parallel improvements in oxidative, inflammatory, and fibrotic parameters measured. The outcomes of cinnamic acid administration were more or less the same as those of pirfenidone. In conclusion, pre-treatment with cinnamic acid protects against methotrexate-induced fibrosis, making it a promising prophylactic adjuvant therapy to methotrexate and protecting against its possible induction of lung fibrosis.© 2023. The Author(s).