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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

Effects of icariin on lung histopathology.Mice were exposed to CS for 3 months and treated with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). Lung tissue was stained by H&E before being examined. (A) The inflammatory cells of lungs measured by bright microscopy (original magnification,×400). (B) The severity of inflammation was calculated on a 0–3 scale defined as described in Materials and methods. Values of MLI (C) and DI (D) were scored also as described in Materials and methods. Data are mean ± SEM (n = 6). *P<0.05 vs. CS-exposed mice. DEX =  dexamethasone; MLI =  mean linear intercepts; DI =  destructive index.
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pone-0102345-g003: Effects of icariin on lung histopathology.Mice were exposed to CS for 3 months and treated with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). Lung tissue was stained by H&E before being examined. (A) The inflammatory cells of lungs measured by bright microscopy (original magnification,×400). (B) The severity of inflammation was calculated on a 0–3 scale defined as described in Materials and methods. Values of MLI (C) and DI (D) were scored also as described in Materials and methods. Data are mean ± SEM (n = 6). *P<0.05 vs. CS-exposed mice. DEX =  dexamethasone; MLI =  mean linear intercepts; DI =  destructive index.

Mentions: Lung tissue was stained using H&E before being examined. We found that (Fig. 3 A, B) there were significant histopathological changes in the airway and the lung parenchyma of CS-exposed mice, including interstitial edema, massive infiltration of the inflammatory cells and pulmonary architecture damage, as compared as controls. Icariin (50 mg/kg and 100 mg/kg) significantly decreased the inflammatory cells in response to CS. However, this effect was not evident in mice treated with dexamethasone.


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)

Effects of icariin on lung histopathology.Mice were exposed to CS for 3 months and treated with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). Lung tissue was stained by H&E before being examined. (A) The inflammatory cells of lungs measured by bright microscopy (original magnification,×400). (B) The severity of inflammation was calculated on a 0–3 scale defined as described in Materials and methods. Values of MLI (C) and DI (D) were scored also as described in Materials and methods. Data are mean ± SEM (n = 6). *P<0.05 vs. CS-exposed mice. DEX =  dexamethasone; MLI =  mean linear intercepts; DI =  destructive index.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0102345-g003: Effects of icariin on lung histopathology.Mice were exposed to CS for 3 months and treated with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). Lung tissue was stained by H&E before being examined. (A) The inflammatory cells of lungs measured by bright microscopy (original magnification,×400). (B) The severity of inflammation was calculated on a 0–3 scale defined as described in Materials and methods. Values of MLI (C) and DI (D) were scored also as described in Materials and methods. Data are mean ± SEM (n = 6). *P<0.05 vs. CS-exposed mice. DEX =  dexamethasone; MLI =  mean linear intercepts; DI =  destructive index.
Mentions: Lung tissue was stained using H&E before being examined. We found that (Fig. 3 A, B) there were significant histopathological changes in the airway and the lung parenchyma of CS-exposed mice, including interstitial edema, massive infiltration of the inflammatory cells and pulmonary architecture damage, as compared as controls. Icariin (50 mg/kg and 100 mg/kg) significantly decreased the inflammatory cells in response to CS. However, this effect was not evident in mice treated with dexamethasone.

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