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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-induced NF-κB activation by BSE. (a) Nuclear NF-κB protein level. Immunoblottings for lamin A verified equal loading and purity of the nuclear proteins. (b) Immunoblottings for phosphorylated I-κBα (p-I-κBα). The cells were treated with LPS or LPS + BSE for 1 h. Immunoblots are representative results from repeated experiments. For (a) and (b), values represent the mean ± S.E.M. (significant as compared with vehicle-treated control, **P < 0.01; significant as compared with LPS alone, ##P < 0.01). BSE: Bojesodok-eum.
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fig6: Inhibition of LPS-induced NF-κB activation by BSE. (a) Nuclear NF-κB protein level. Immunoblottings for lamin A verified equal loading and purity of the nuclear proteins. (b) Immunoblottings for phosphorylated I-κBα (p-I-κBα). The cells were treated with LPS or LPS + BSE for 1 h. Immunoblots are representative results from repeated experiments. For (a) and (b), values represent the mean ± S.E.M. (significant as compared with vehicle-treated control, **P < 0.01; significant as compared with LPS alone, ##P < 0.01). BSE: Bojesodok-eum.

Mentions: NF-κB is the key transcription factor for the inflammatory genes such as iNOS and COX-2 and activated in immune cells stimulated by LPS or other inflammatory challenges [10–12]. Translocation of NF-κB to the nucleus is permitted by phosphorylation of I-κBα and degradation of I-κBα subunit. We then assessed the nuclear level of NF-κB in the cells treated with LPS with or without BSE. The treatment of BSE in RAW 264.7 cells significantly inhibited LPS-inducible increase in nuclear level of NF-κB (Figure 6(a)). Furthermore, exposure of LPS increased phosphorylation of I-κBα, which was also blocked subsequent treatment of BSE (Figure 6(b)). Thus, BSE might prevent iNOS and COX-2 gene induction by inhibiting NF-κB activation.


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-induced NF-κB activation by BSE. (a) Nuclear NF-κB protein level. Immunoblottings for lamin A verified equal loading and purity of the nuclear proteins. (b) Immunoblottings for phosphorylated I-κBα (p-I-κBα). The cells were treated with LPS or LPS + BSE for 1 h. Immunoblots are representative results from repeated experiments. For (a) and (b), values represent the mean ± S.E.M. (significant as compared with vehicle-treated control, **P < 0.01; significant as compared with LPS alone, ##P < 0.01). BSE: Bojesodok-eum.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3472669&req=5

fig6: Inhibition of LPS-induced NF-κB activation by BSE. (a) Nuclear NF-κB protein level. Immunoblottings for lamin A verified equal loading and purity of the nuclear proteins. (b) Immunoblottings for phosphorylated I-κBα (p-I-κBα). The cells were treated with LPS or LPS + BSE for 1 h. Immunoblots are representative results from repeated experiments. For (a) and (b), values represent the mean ± S.E.M. (significant as compared with vehicle-treated control, **P < 0.01; significant as compared with LPS alone, ##P < 0.01). BSE: Bojesodok-eum.
Mentions: NF-κB is the key transcription factor for the inflammatory genes such as iNOS and COX-2 and activated in immune cells stimulated by LPS or other inflammatory challenges [10–12]. Translocation of NF-κB to the nucleus is permitted by phosphorylation of I-κBα and degradation of I-κBα subunit. We then assessed the nuclear level of NF-κB in the cells treated with LPS with or without BSE. The treatment of BSE in RAW 264.7 cells significantly inhibited LPS-inducible increase in nuclear level of NF-κB (Figure 6(a)). Furthermore, exposure of LPS increased phosphorylation of I-κBα, which was also blocked subsequent treatment of BSE (Figure 6(b)). Thus, BSE might prevent iNOS and COX-2 gene induction by inhibiting NF-κB activation.

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