ArticleACS pharmacology & translational science2025
Ferulic Acid Attenuated Interleukin-17A-Induced Lung Inflammation by Modulating Interleukin-17 Signaling and Tissue Remodeling in a Mouse Model.
Article in ACS pharmacology & translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Lung inflammation is a hallmark of several respiratory diseases and is frequently driven by proinflammatory cytokines such as interleukin-17A (IL-17A). IL-17A plays a critical role in amplifying inflammatory cascades, contributing to airway remodeling and tissue damage. This study investigated the therapeutic potential of ferulic acid (FA), a natural polyphenol with known antioxidant and anti-inflammatory properties, in mitigating recombinant IL-17A (rmIL-17A)-induced lung inflammation in BALB/c mice. Mice were intranasally exposed to rmIL-17A for seven consecutive days, while FA was administered orally from day 4 to day 7. FA treatment significantly downregulated IL-17A-mediated signaling pathways and restored the redox balance disrupted by rmIL-17A exposure. Additionally, FA markedly reduced proinflammatory cytokine levels, inflammatory cell infiltration, mast cell activity, mucus hypersecretion, and fibrosis in the lung tissue. Importantly, FA also decreased the expression of CD38 and restored CD206 expression, indicating a phenotypic shift toward anti-inflammatory macrophage polarization. Interestingly, FA also restored the expression level of occludin in the lungs of mice exposed to rmIL-17A. Overall, these findings demonstrate that FA effectively attenuates IL-17A-induced lung inflammation by modulating oxidative stress, cytokine production, and inflammatory cell responses. These outcomes show the potential of FA as a promising therapeutic option for regulating IL-17A-driven pulmonary inflammatory conditions.
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