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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 inhibits NF-κB activation in CS-induced inflammation.Mice were exposed to CS for 3 months and dosed with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). (A) Nuclear proteins were extracted from lung tissue and p65, p-p65 and IκB-α protein expression was measured by Western blot. The phosphorylation of p65 (B) and the degradation of IκB-α (C) were calculated using gray value ratio of p65/p-p65 and IκB-α/GAPDH, respectively. Data are mean ± SEM (n = 3). * P<0.05 vs. CS-exposed mice.
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pone-0102345-g005: Icariin inhibits NF-κB activation in CS-induced inflammation.Mice were exposed to CS for 3 months and dosed with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). (A) Nuclear proteins were extracted from lung tissue and p65, p-p65 and IκB-α protein expression was measured by Western blot. The phosphorylation of p65 (B) and the degradation of IκB-α (C) were calculated using gray value ratio of p65/p-p65 and IκB-α/GAPDH, respectively. Data are mean ± SEM (n = 3). * P<0.05 vs. CS-exposed mice.

Mentions: Based on our previous findings that icariin inhibiting the LPS-induced NF-κB activation in vivo and in vitro[16], we also investigated whether icariin could interfere with the NF-κB activation in lungs of CS-exposed mice. As shown in Fig. 5, 3 months of CS-exposure markedly (P<0.05) increased the phosphorylation of nuclear NF-κB p65 and the degradation of IκB-α. Icariin apparently (P<0.05) inhibited the expression of p65 protein phosphorylation and blocked the degradation of IκB-α, indicating that icariin had inhibitory effect on CSE-activated NF-κB pathway.


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 inhibits NF-κB activation in CS-induced inflammation.Mice were exposed to CS for 3 months and dosed with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). (A) Nuclear proteins were extracted from lung tissue and p65, p-p65 and IκB-α protein expression was measured by Western blot. The phosphorylation of p65 (B) and the degradation of IκB-α (C) were calculated using gray value ratio of p65/p-p65 and IκB-α/GAPDH, respectively. Data are mean ± SEM (n = 3). * P<0.05 vs. CS-exposed mice.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0102345-g005: Icariin inhibits NF-κB activation in CS-induced inflammation.Mice were exposed to CS for 3 months and dosed with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). (A) Nuclear proteins were extracted from lung tissue and p65, p-p65 and IκB-α protein expression was measured by Western blot. The phosphorylation of p65 (B) and the degradation of IκB-α (C) were calculated using gray value ratio of p65/p-p65 and IκB-α/GAPDH, respectively. Data are mean ± SEM (n = 3). * P<0.05 vs. CS-exposed mice.
Mentions: Based on our previous findings that icariin inhibiting the LPS-induced NF-κB activation in vivo and in vitro[16], we also investigated whether icariin could interfere with the NF-κB activation in lungs of CS-exposed mice. As shown in Fig. 5, 3 months of CS-exposure markedly (P<0.05) increased the phosphorylation of nuclear NF-κB p65 and the degradation of IκB-α. Icariin apparently (P<0.05) inhibited the expression of p65 protein phosphorylation and blocked the degradation of IκB-α, indicating that icariin had inhibitory effect on CSE-activated NF-κB pathway.

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