Icariin Ameliorates Cigarette Smoke Induced Inflammatory Responses via Suppression of NF-κB and Modulation of GR In Vivo and In Vitro
Author(s) -
Lulu Li,
Jing Sun,
Changqing Xu,
Hongying Zhang,
Jinfeng Wu,
Baojun Liu,
Jingcheng Dong
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0102345
Subject(s) - icariin , in vivo , in vitro , chemistry , nf κb , inflammatory response , inflammation , pharmacology , cigarette smoke , microbiology and biotechnology , medicine , signal transduction , biology , immunology , biochemistry , toxicology , pathology , alternative medicine
Purpose To investigate the effects of icariin, a major constituent of flavonoids isolated from the herb Epimedium , on cigarette smoke (CS) induced inflammatory responses in vivo and in vitro . Methods In vivo , BALB/c mice were exposed to smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months and dosed with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). In vitro , A549 cells were incubated with icariin (10, 50 and 100 µM) followed by treatments with CSE (2.5%). Results We found that icariin significantly protected pulmonary function and attenuated CS-induced inflammatory response by decreasing inflammatory cells and production of TNF-α, IL-8 and MMP-9 in both the serum and BALF of CS-exposed mice and decreasing production of TNF-α and IL-8 in the supernatant of CSE-exposed A549 cells. Icariin also showed properties in inhibiting the phosphorylation of NF-κB p65 protein and blocking the degradation of IΚB-α protein. Further studies revealed that icariin administration markedly restore CS-reduced GR protein and mRNA expression, which might subsequently contribute to the attenuation of CS-induced respiratory inflammatory response. Conclusion Together these results suggest that icariin has anti-inflammatory effects in cigarette smoke induced inflammatory models in vivo and in vitro , possibly achieved by suppressing NF-κB activation and modulating GR protein expression.
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