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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 iNOS and COX-2 by BSE. (a) iNOS and COX-2, immunoblottings (upper). iNOS, COX-2, or COX-1 protein levels were monitored 12 h after treatment with LPS (1 μg/mL). Relative iNOS and COX-2 protein levels of the upper immunoblottings (lower). Values represent the mean ± S.E.M. (significantly different as compared to LPS-treated group, *P < 0.05, *P < 0.01). (b) Inhibition of LPS-inducible COX activity by BSE. The COX, COX-1, or COX-2 enzyme activity was measured as described in the Methods section. Data represents the mean ± S.E.M. from three separate experiments (significant as compared with LPS alone, ##P < 0.01). BSE: Bojesodok-eum.
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fig5: Inhibition of LPS-inducible iNOS and COX-2 by BSE. (a) iNOS and COX-2, immunoblottings (upper). iNOS, COX-2, or COX-1 protein levels were monitored 12 h after treatment with LPS (1 μg/mL). Relative iNOS and COX-2 protein levels of the upper immunoblottings (lower). Values represent the mean ± S.E.M. (significantly different as compared to LPS-treated group, *P < 0.05, *P < 0.01). (b) Inhibition of LPS-inducible COX activity by BSE. The COX, COX-1, or COX-2 enzyme activity was measured as described in the Methods section. Data represents the mean ± S.E.M. from three separate experiments (significant as compared with LPS alone, ##P < 0.01). BSE: Bojesodok-eum.

Mentions: Next, we assessed the protein expression of iNOS and COX-2 by western blotting. LPS treatment markedly induced iNOS and COX-2, whereas BSE treatment (10–100 μL/mL) prevented the iNOS and COX-2 induction (Figure 5(a), upper). BSE also inhibited COX-1 induction by LPS. Although BSE treatment almost completely abrogated LPS-induced iNOS, analysis using densitometer revealed that ability of BSE to inhibit COX-2 and COX-1 expressions was less potent than its effect on iNOS (Figure 5(a), lower). Therefore, we examined the effect of BSE on COX activity. Interestingly, treatment of BSE (10–100 μL/mL) significantly inhibited LPS-inducible COX activity (Figure 5(b)). Moreover, COX-1 and COX-2 activity were also prevented by BSE treatment (Figure 5(b)). This data confirmed that BSE treatment inhibits iNOS and COX-2 expression as well as COX-2 enzyme activity.


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 iNOS and COX-2 by BSE. (a) iNOS and COX-2, immunoblottings (upper). iNOS, COX-2, or COX-1 protein levels were monitored 12 h after treatment with LPS (1 μg/mL). Relative iNOS and COX-2 protein levels of the upper immunoblottings (lower). Values represent the mean ± S.E.M. (significantly different as compared to LPS-treated group, *P < 0.05, *P < 0.01). (b) Inhibition of LPS-inducible COX activity by BSE. The COX, COX-1, or COX-2 enzyme activity was measured as described in the Methods section. Data represents the mean ± S.E.M. from three separate experiments (significant as compared with LPS alone, ##P < 0.01). BSE: Bojesodok-eum.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig5: Inhibition of LPS-inducible iNOS and COX-2 by BSE. (a) iNOS and COX-2, immunoblottings (upper). iNOS, COX-2, or COX-1 protein levels were monitored 12 h after treatment with LPS (1 μg/mL). Relative iNOS and COX-2 protein levels of the upper immunoblottings (lower). Values represent the mean ± S.E.M. (significantly different as compared to LPS-treated group, *P < 0.05, *P < 0.01). (b) Inhibition of LPS-inducible COX activity by BSE. The COX, COX-1, or COX-2 enzyme activity was measured as described in the Methods section. Data represents the mean ± S.E.M. from three separate experiments (significant as compared with LPS alone, ##P < 0.01). BSE: Bojesodok-eum.
Mentions: Next, we assessed the protein expression of iNOS and COX-2 by western blotting. LPS treatment markedly induced iNOS and COX-2, whereas BSE treatment (10–100 μL/mL) prevented the iNOS and COX-2 induction (Figure 5(a), upper). BSE also inhibited COX-1 induction by LPS. Although BSE treatment almost completely abrogated LPS-induced iNOS, analysis using densitometer revealed that ability of BSE to inhibit COX-2 and COX-1 expressions was less potent than its effect on iNOS (Figure 5(a), lower). Therefore, we examined the effect of BSE on COX activity. Interestingly, treatment of BSE (10–100 μL/mL) significantly inhibited LPS-inducible COX activity (Figure 5(b)). Moreover, COX-1 and COX-2 activity were also prevented by BSE treatment (Figure 5(b)). This data confirmed that BSE treatment inhibits iNOS and COX-2 expression as well as COX-2 enzyme activity.

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