Turmeric extract alleviates airway inflammation via oxidative stress-driven MAPKs/MMPs pathway

被引:0
|
作者
Kim, Jeong-Won [1 ]
Jeong, Ji-Soo [1 ]
Kim, Jin-Hwa [1 ]
Kim, Chang-Yeop [1 ]
Chung, Eun-Hye [1 ]
Ko, Je-Won [1 ]
Kim, Tae-Won [1 ]
机构
[1] Chungnam Natl Univ, Coll Vet Med, BK21 FOUR Program, 99 Daehak-ro, Daejeon 34131, South Korea
基金
新加坡国家研究基金会;
关键词
Turmeric; Asthma; Oxidative stress; Mitogen-activated protein kinase; Matrix metalloproteinase-9; MOLECULAR-MECHANISMS; SIGNALING PATHWAYS; MMP-9; EXPRESSION; P38; MAPK; ASTHMA; CYTOKINES; CURCUMIN; MATRIX-METALLOPROTEINASE-9; INHIBITOR; MODEL;
D O I
10.1016/j.intimp.2024.113018
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Turmeric (Curcuma longa L.) extract (CLE) has been shown to elicit several pharmacological properties and is widely used in Asian traditional medicine. Herein, we assessed the impact of CLE on airway inflammation in BALB/c mice and A549 cells to clarify the underlying mechanism. An asthmatic mouse model was established by administering ovalbumin (OVA). CLE (100 or 300 mg/kg/day) was orally administered daily from days 18 to 23, with dexamethasone (3 mg/kg/day) used as the positive control. Human airway epithelial cells, A549, were stimulated using recombinant tumor necrosis factor-alpha. The CLE100 and CLE400 groups exhibited a significant downregulation in eosinophil counts, cytokine levels, and immunoglobulin-E levels. Moreover, CLE administration dose-dependently suppressed oxidative stress and airway inflammation in the lung tissue. CLE administration inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) and the expression and activity of matrix metalloproteinase (MMP)-9. In vitro, CLE treatment reduced mRNA levels of proinflammatory cytokines, MAPK phosphorylation, and the expression and activity of MMP-2 and MMP-9. Additionally, 50 mu g/ mL CLE and 2.5 mu g/mL curcumin showed similar anti-inflammatory effects. Collectively, our findings revealed that CLE could suppress airway inflammation in asthmatic mice and A549 cells via oxidative stress-driven MAPK/MMPs signaling, suggesting that CLE could be developed as a potential treatment option for patients with asthma.
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页数:10
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