Codium fragile Extract Ameliorates Respiratory Function by Controlling Allergic Inflammation in Ovalbumin-Induced Bronchial Disorders in Miceopen access
- Authors
- Lee, Hyo Lim; Ju, Yeong Hyeon; Kim, In Young; Choi, Hye Ji; Heo, Yu Mi; Na, Hwa Rang; Heo, Ho Jin
- Issue Date
- May-2025
- Publisher
- Multidisciplinary Digital Publishing Institute (MDPI)
- Keywords
- Codium fragile; oleamide; allergic inflammation; Th2 cytokine; fibrosis; pulmonary function
- Citation
- Marine Drugs, v.23, no.5
- Indexed
- SCIE
SCOPUS
- Journal Title
- Marine Drugs
- Volume
- 23
- Number
- 5
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/78721
- DOI
- 10.3390/md23050221
- ISSN
- 1660-3397
1660-3397
- Abstract
- This study investigated the effect of Codium fragile (WCF) water extract in reducing allergic inflammation in ovalbumin (OVA)-induced mice. Mice were sensitized to OVA + aluminum hydroxide, administered WCF for one week, and exposed to 1% aerosolized OVA. As a result, WCF intake reduced the OVA-induced increase in CD4+ T cells, CD8+ T cells, the T helper type 2 (Th2)/T helper type 1 (Th1) cell ratio, and inflammatory cells such as eosinophils and lymphocytes. Furthermore, WCF reduced Th2 cytokines such as interleukin (IL)-5, IL-13, and IL-33 and inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and IL-1 beta in lung tissues. A histological analysis showed that WCF intake decreases OVA-induced pulmonary inflammation, bronchial wall thickness, and mucus score and increases pulmonary alveolar area. Moreover, WCF inhibited the nuclear factor kappa B (NF-kappa B) pathway, the transforming growth factor beta (TGF-beta)/Smad pathway, and apoptosis-related proteins in lung tissues that OVA excessively activated. The oleamide (9-octadecenamide) content, representing a physiologically active component of WCF, was analyzed and validated using a high-performance liquid chromatography-photodiode array (HPLC-PDA) system. These results demonstrate that WCF may serve as a potential preventive agent for respiratory dysfunction such as allergic asthma by suppressing NF-kappa B and TGF-beta/Smad pathways.
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