Abstract
PurposeTo 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%).ResultsWe 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.ConclusionTogether 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.
Highlights
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease that is characterized by airway obstruction and progressive lung inflammation that is associated with the influx of inflammatory cells such as neutrophils, macrophages, lymphocytes and epithelial cells [1,2], as well as increases in the levels of a complex cascade of inflammatory mediators including chemokines such as IL-8 and pro-inflammatory cytokines such as tumor necrosis factor-a (TNF-a), IL-1b, IL-6 and MMP-9 [3,4]
The molecular mechanisms that underlying the inflammation with glucocorticoid insensitivity in COPD are currently still unclear, but a possible explanation may involve the impaired ability of glucocorticoid receptor (GR) [10], which mediates the effect of glucocorticoid by translocating into the nucleus, binding to glucocorticoid responsive elements (GRE) in the DNA or with the transcription factors activating protein-1 (AP1) and nuclear factor-kB (NF-kB), thereby preventing inflammatory gene expression [11,12]
To examine whether icariin restored pulmonary function in CSexposed mice, breathing parameters were determined by wholebody barometric plethysmography after 3 months of exposure to air or cigarette smoke
Summary
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease that is characterized by airway obstruction and progressive lung inflammation that is associated with the influx of inflammatory cells such as neutrophils, macrophages, lymphocytes and epithelial cells [1,2], as well as increases in the levels of a complex cascade of inflammatory mediators including chemokines such as IL-8 and pro-inflammatory cytokines such as TNF-a, IL-1b, IL-6 and MMP-9 [3,4]. In view of the inflammation with glucocorticoid insensitivity in COPD, there is a pressing need for the development of effective anti-inflammatory drugs
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