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Icariin ameliorates cigarette smoke induced inflammatory responses via suppression of NF-κB and modulation of GR in vivo and in vitro.

Li L, Sun J, Xu C, Zhang H, Wu J, Liu B, Dong J - PLoS ONE (2014)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Integrated Traditional Chinese and Western Medicine, Huashan Hospital, Fudan University, Shanghai, China.

ABSTRACT

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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Related in: MedlinePlus

Icariin suppresses CS-induced TNF-α, IL-8 and MMP-9 levels in vivo and in vitro.TNF-α, IL-8 and MMP-9 levels in serum (A), BALF (B) and culture supernatant (C) were measured by ELISA. Data are mean ± SEM (n = 4–5). * P<0.05 vs. CS-exposed mice or CSE-exposed A549 cells. CS = cigarette smoke; CSE = cigarette smoke extract; DEX =  dexamethasone; BALF  = bronchoalveolar lavage.
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pone-0102345-g004: Icariin suppresses CS-induced TNF-α, IL-8 and MMP-9 levels in vivo and in vitro.TNF-α, IL-8 and MMP-9 levels in serum (A), BALF (B) and culture supernatant (C) were measured by ELISA. Data are mean ± SEM (n = 4–5). * P<0.05 vs. CS-exposed mice or CSE-exposed A549 cells. CS = cigarette smoke; CSE = cigarette smoke extract; DEX =  dexamethasone; BALF  = bronchoalveolar lavage.

Mentions: To further characterize the effects of icariin on modulating inflammatory response to cigarette smoke exposure in mice lungs and supernatants of A549 cells, we analyzed some inflammatory cytokines. As shown in Fig. 4A and B, significant (P<0.05) increases of TNF-α, IL-8 and MMP-9 levels in both BALF and serum were observed following treatment with 3 months of CS-exposure compared with controls. Treatments with icariin (25 mg/kg, 50 mg/kg, 100 mg/kg) significantly (P<0.05) inhibited TNF-α, IL-8 and MMP-9 production in serum compared with CS-exposed mice. In contrast, dexamethasone significantly reduced production of TNF-α and IL-8 compared with CS-exposed mice, but failed to (P>0.05) suppress the elevated levels of MMP-9 (Fig. 4A). A similar response was also observed in BALF (Fig. 4B). Furthermore, our in vitro experiments also showed that middle and high concentrations of icariin (10 µM and 50 µM) obviously (P<0.05) suppressed CSE-elevated productions of IL-8 and TNF-α in supernatant of A549 cells (Fig. 4C).


Icariin ameliorates cigarette smoke induced inflammatory responses via suppression of NF-κB and modulation of GR in vivo and in vitro.

Li L, Sun J, Xu C, Zhang H, Wu J, Liu B, Dong J - PLoS ONE (2014)

Icariin suppresses CS-induced TNF-α, IL-8 and MMP-9 levels in vivo and in vitro.TNF-α, IL-8 and MMP-9 levels in serum (A), BALF (B) and culture supernatant (C) were measured by ELISA. Data are mean ± SEM (n = 4–5). * P<0.05 vs. CS-exposed mice or CSE-exposed A549 cells. CS = cigarette smoke; CSE = cigarette smoke extract; DEX =  dexamethasone; BALF  = bronchoalveolar lavage.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4121073&req=5

pone-0102345-g004: Icariin suppresses CS-induced TNF-α, IL-8 and MMP-9 levels in vivo and in vitro.TNF-α, IL-8 and MMP-9 levels in serum (A), BALF (B) and culture supernatant (C) were measured by ELISA. Data are mean ± SEM (n = 4–5). * P<0.05 vs. CS-exposed mice or CSE-exposed A549 cells. CS = cigarette smoke; CSE = cigarette smoke extract; DEX =  dexamethasone; BALF  = bronchoalveolar lavage.
Mentions: To further characterize the effects of icariin on modulating inflammatory response to cigarette smoke exposure in mice lungs and supernatants of A549 cells, we analyzed some inflammatory cytokines. As shown in Fig. 4A and B, significant (P<0.05) increases of TNF-α, IL-8 and MMP-9 levels in both BALF and serum were observed following treatment with 3 months of CS-exposure compared with controls. Treatments with icariin (25 mg/kg, 50 mg/kg, 100 mg/kg) significantly (P<0.05) inhibited TNF-α, IL-8 and MMP-9 production in serum compared with CS-exposed mice. In contrast, dexamethasone significantly reduced production of TNF-α and IL-8 compared with CS-exposed mice, but failed to (P>0.05) suppress the elevated levels of MMP-9 (Fig. 4A). A similar response was also observed in BALF (Fig. 4B). Furthermore, our in vitro experiments also showed that middle and high concentrations of icariin (10 µM and 50 µM) obviously (P<0.05) suppressed CSE-elevated productions of IL-8 and TNF-α in supernatant of A549 cells (Fig. 4C).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Integrated Traditional Chinese and Western Medicine, Huashan Hospital, Fudan University, Shanghai, China.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus