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Bojesodok-eum, a Herbal Prescription, Ameliorates Acute Inflammation in Association with the Inhibition of NF-κB-Mediated Nitric Oxide and ProInflammatory Cytokine Production.

Sohn KH, Jo MJ, Cho WJ, Lee JR, Cho IJ, Kim SC, Kim YW, Jee SY - Evid Based Complement Alternat Med (2012)

Bottom Line: In cell model, treatment of BSE decreased the production of NO and PGE(2) in RAW264.7 cells stimulated by LPS.BSE also inhibited the expression of iNOS and COX-2 protein as well as COX activity in a concentration-dependent manner.LPS treatment induced nuclear NF-κB level and I-κBα phosphorylation, which were inhibited subsequent treatment of BSE, suggesting its repression of LPS-inducible NF-κB activation.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Otolaryngology and Dermatology, College of Oriental Medicine, Daegu Haany University, Daegu 706-828, Republic of Korea.

ABSTRACT
Bojesodok-eum (BSE) is a herbal prescription consisting of Coptidis Rhizoma and Scutellariae Radix as main components. This paper investigated the effects of BSE on the induction of nitric oxide (NO), prostaglandin E(2) (PGE(2)), and proinflammatory cytokines that are caused by lipopolysaccharide (LPS) in murine macrophage cell line and on the paw edema formation in animals. Administration of BSE (0.3 g/kg and 1 g/kg) in rats significantly inhibited carrageenan-induced paw edema formation, as did dexamethasone, an anti-inflammatory positive control drug. In cell model, treatment of BSE decreased the production of NO and PGE(2) in RAW264.7 cells stimulated by LPS. BSE also inhibited the expression of iNOS and COX-2 protein as well as COX activity in a concentration-dependent manner. Consistently, BSE suppressed the ability of LPS to produce TNF-α, interleukin-1β, and interleukin-6. LPS treatment induced nuclear NF-κB level and I-κBα phosphorylation, which were inhibited subsequent treatment of BSE, suggesting its repression of LPS-inducible NF-κB activation. BSE abrogated the induction of NO, PGE(2), and proinflammatory cytokines, as well as iNOS and COX-2 protein expression in RAW264.7 cells stimulated by LPS as mediated with NF-κB inhibition.

No MeSH data available.


Related in: MedlinePlus

Inhibition of LPS-inducible TNF-α, IL-1β, and IL-6 by BSE. (a) TNF-α, (b) IL-1β, and (c) IL-6 contents in culture medium. RAW264.7 cells were treated with 10, 30, and 100 μg/mL BSE for the 1 h and continuously incubated with LPS (1 μg/mL) for 24 h. Data represents the mean ± S.E.M. from three separate experiments (significant as compared with vehicle-treated control, **P < 0.01; significant as compared with LPS alone, ##P < 0.05, ##P < 0.01). BSE: Bojesodok-eum.
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fig4: Inhibition of LPS-inducible TNF-α, IL-1β, and IL-6 by BSE. (a) TNF-α, (b) IL-1β, and (c) IL-6 contents in culture medium. RAW264.7 cells were treated with 10, 30, and 100 μg/mL BSE for the 1 h and continuously incubated with LPS (1 μg/mL) for 24 h. Data represents the mean ± S.E.M. from three separate experiments (significant as compared with vehicle-treated control, **P < 0.01; significant as compared with LPS alone, ##P < 0.05, ##P < 0.01). BSE: Bojesodok-eum.

Mentions: Cytokines are the major regulator in inflammatory responses and released by injured or infected cells. Next, we verified the effects of BSE on proinflammatory cytokines including TNF-α, IL-1β, and IL-6. We measured production of the cytokines in the media of RAW264.7 cells by using ELISA assays. LPS stimulation significantly increased the production of the cytokines (Figures 4(a)–4(c)). Concomitant treatment of BSE blocked the ability of LPS to increase the proinflammatory cytokine productions.


Bojesodok-eum, a Herbal Prescription, Ameliorates Acute Inflammation in Association with the Inhibition of NF-κB-Mediated Nitric Oxide and ProInflammatory Cytokine Production.

Sohn KH, Jo MJ, Cho WJ, Lee JR, Cho IJ, Kim SC, Kim YW, Jee SY - Evid Based Complement Alternat Med (2012)

Inhibition of LPS-inducible TNF-α, IL-1β, and IL-6 by BSE. (a) TNF-α, (b) IL-1β, and (c) IL-6 contents in culture medium. RAW264.7 cells were treated with 10, 30, and 100 μg/mL BSE for the 1 h and continuously incubated with LPS (1 μg/mL) for 24 h. Data represents the mean ± S.E.M. from three separate experiments (significant as compared with vehicle-treated control, **P < 0.01; significant as compared with LPS alone, ##P < 0.05, ##P < 0.01). BSE: Bojesodok-eum.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3472669&req=5

fig4: Inhibition of LPS-inducible TNF-α, IL-1β, and IL-6 by BSE. (a) TNF-α, (b) IL-1β, and (c) IL-6 contents in culture medium. RAW264.7 cells were treated with 10, 30, and 100 μg/mL BSE for the 1 h and continuously incubated with LPS (1 μg/mL) for 24 h. Data represents the mean ± S.E.M. from three separate experiments (significant as compared with vehicle-treated control, **P < 0.01; significant as compared with LPS alone, ##P < 0.05, ##P < 0.01). BSE: Bojesodok-eum.
Mentions: Cytokines are the major regulator in inflammatory responses and released by injured or infected cells. Next, we verified the effects of BSE on proinflammatory cytokines including TNF-α, IL-1β, and IL-6. We measured production of the cytokines in the media of RAW264.7 cells by using ELISA assays. LPS stimulation significantly increased the production of the cytokines (Figures 4(a)–4(c)). Concomitant treatment of BSE blocked the ability of LPS to increase the proinflammatory cytokine productions.

Bottom Line: In cell model, treatment of BSE decreased the production of NO and PGE(2) in RAW264.7 cells stimulated by LPS.BSE also inhibited the expression of iNOS and COX-2 protein as well as COX activity in a concentration-dependent manner.LPS treatment induced nuclear NF-κB level and I-κBα phosphorylation, which were inhibited subsequent treatment of BSE, suggesting its repression of LPS-inducible NF-κB activation.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Otolaryngology and Dermatology, College of Oriental Medicine, Daegu Haany University, Daegu 706-828, Republic of Korea.

ABSTRACT
Bojesodok-eum (BSE) is a herbal prescription consisting of Coptidis Rhizoma and Scutellariae Radix as main components. This paper investigated the effects of BSE on the induction of nitric oxide (NO), prostaglandin E(2) (PGE(2)), and proinflammatory cytokines that are caused by lipopolysaccharide (LPS) in murine macrophage cell line and on the paw edema formation in animals. Administration of BSE (0.3 g/kg and 1 g/kg) in rats significantly inhibited carrageenan-induced paw edema formation, as did dexamethasone, an anti-inflammatory positive control drug. In cell model, treatment of BSE decreased the production of NO and PGE(2) in RAW264.7 cells stimulated by LPS. BSE also inhibited the expression of iNOS and COX-2 protein as well as COX activity in a concentration-dependent manner. Consistently, BSE suppressed the ability of LPS to produce TNF-α, interleukin-1β, and interleukin-6. LPS treatment induced nuclear NF-κB level and I-κBα phosphorylation, which were inhibited subsequent treatment of BSE, suggesting its repression of LPS-inducible NF-κB activation. BSE abrogated the induction of NO, PGE(2), and proinflammatory cytokines, as well as iNOS and COX-2 protein expression in RAW264.7 cells stimulated by LPS as mediated with NF-κB inhibition.

No MeSH data available.


Related in: MedlinePlus