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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 NO and PGE2 by BSE. (a) MTT assay. RAW264.7 cells were treated with 10, 30, 100, and 300 μg/mL BSE for 1 h and continuously incubated with LPS (1 μg/mL). (b) NO and (c) PGE2 productions. RAW264.7 cells were treated with BSE at the indicated concentration for 1 h and continuously incubated with LPS (1 μg/mL) for the next 24 h. NO and PGE2 concentration in culture media was monitored, as described in the Methods section. 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 < 0.01). N.S. not significant; BSE: Bojesodok-eum.
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fig3: Inhibition of LPS-inducible NO and PGE2 by BSE. (a) MTT assay. RAW264.7 cells were treated with 10, 30, 100, and 300 μg/mL BSE for 1 h and continuously incubated with LPS (1 μg/mL). (b) NO and (c) PGE2 productions. RAW264.7 cells were treated with BSE at the indicated concentration for 1 h and continuously incubated with LPS (1 μg/mL) for the next 24 h. NO and PGE2 concentration in culture media was monitored, as described in the Methods section. 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 < 0.01). N.S. not significant; BSE: Bojesodok-eum.

Mentions: This study was extended to verify anti-inflammatory effect of BSE in a cell model. To test cellular toxicity of BSE, MTT assay was assessed in RAW 264.7 cells. Figure 3(a) showed that cell survival was not affected by BSE treatment up to 300 μg/mL. Next, we assessed the effect of BSE (10–300 μL/mL) on NO and PGE2 production in RAW264.7 cells. NO and PGE2 productions were measured in the media of RAW264.7 cells treated with LPS and/or BSE as described in Method section. LPS treatment for 24 h increased NO production by 160% compared to control, which was inhibited by treatment of BSE (Figure 3(b)). In the subsequent experiments, we chose 10–100 μg/mL concentrations of BSE to verify its effect on PGE2 production. BSE treatment markedly blocked PGE2 production in RAW 264.7 cell stimulated with LPS (Figure 3(c)).


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 NO and PGE2 by BSE. (a) MTT assay. RAW264.7 cells were treated with 10, 30, 100, and 300 μg/mL BSE for 1 h and continuously incubated with LPS (1 μg/mL). (b) NO and (c) PGE2 productions. RAW264.7 cells were treated with BSE at the indicated concentration for 1 h and continuously incubated with LPS (1 μg/mL) for the next 24 h. NO and PGE2 concentration in culture media was monitored, as described in the Methods section. 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 < 0.01). N.S. not significant; BSE: Bojesodok-eum.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig3: Inhibition of LPS-inducible NO and PGE2 by BSE. (a) MTT assay. RAW264.7 cells were treated with 10, 30, 100, and 300 μg/mL BSE for 1 h and continuously incubated with LPS (1 μg/mL). (b) NO and (c) PGE2 productions. RAW264.7 cells were treated with BSE at the indicated concentration for 1 h and continuously incubated with LPS (1 μg/mL) for the next 24 h. NO and PGE2 concentration in culture media was monitored, as described in the Methods section. 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 < 0.01). N.S. not significant; BSE: Bojesodok-eum.
Mentions: This study was extended to verify anti-inflammatory effect of BSE in a cell model. To test cellular toxicity of BSE, MTT assay was assessed in RAW 264.7 cells. Figure 3(a) showed that cell survival was not affected by BSE treatment up to 300 μg/mL. Next, we assessed the effect of BSE (10–300 μL/mL) on NO and PGE2 production in RAW264.7 cells. NO and PGE2 productions were measured in the media of RAW264.7 cells treated with LPS and/or BSE as described in Method section. LPS treatment for 24 h increased NO production by 160% compared to control, which was inhibited by treatment of BSE (Figure 3(b)). In the subsequent experiments, we chose 10–100 μg/mL concentrations of BSE to verify its effect on PGE2 production. BSE treatment markedly blocked PGE2 production in RAW 264.7 cell stimulated with LPS (Figure 3(c)).

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