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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 baicalin. (A) NO and (B) PGE2 productions. RAW264.7 cells were treated with baicalin or berberine at the indicated concentration for 1 h and LPS (1 μg/mL) for the next 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 < 0.01).
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fig8: Inhibition of LPS-inducible NO and PGE2 by baicalin. (A) NO and (B) PGE2 productions. RAW264.7 cells were treated with baicalin or berberine at the indicated concentration for 1 h and LPS (1 μg/mL) for the next 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 < 0.01).

Mentions: Coptidis Rhizoma and Scutellariae Radix are two main herbs in the BSE. Therefore, we used the UPLC system in determination of four markers, baicalin, baicalein, berberine, and wogonin, which are the major components in Coptidis Rhizoma (i.e., berberine) and Scutellariae Radix (i.e., baicalin, baicalein and wogonin) [25, 26]. Contents of the four marker components were calculated from the calibration curve of the standards using UPLC (Table 3 and Figures 7(A) and 7(B)), indicating baicalin and berberine are most enriched compounds in BSE. Therefore, we determined the effects of baicalin, and berberine on the LPS-inducible NO and PGE2 accumulation in RAW264.7 cells. Baicalin treatment (3 and 10 μM) markedly inhibited NO and PGE2 productions induced by LPS (Figures 8(a) and 8(b)). On the other hand, 3 and 10 μM treatment of berberine failed to decrease in the NO induction, and, significantly, but less potently than baicalin, blocked PGE2 accumulation (Figures 8(a) and 8(b)).


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 baicalin. (A) NO and (B) PGE2 productions. RAW264.7 cells were treated with baicalin or berberine at the indicated concentration for 1 h and LPS (1 μg/mL) for the next 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 < 0.01).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig8: Inhibition of LPS-inducible NO and PGE2 by baicalin. (A) NO and (B) PGE2 productions. RAW264.7 cells were treated with baicalin or berberine at the indicated concentration for 1 h and LPS (1 μg/mL) for the next 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 < 0.01).
Mentions: Coptidis Rhizoma and Scutellariae Radix are two main herbs in the BSE. Therefore, we used the UPLC system in determination of four markers, baicalin, baicalein, berberine, and wogonin, which are the major components in Coptidis Rhizoma (i.e., berberine) and Scutellariae Radix (i.e., baicalin, baicalein and wogonin) [25, 26]. Contents of the four marker components were calculated from the calibration curve of the standards using UPLC (Table 3 and Figures 7(A) and 7(B)), indicating baicalin and berberine are most enriched compounds in BSE. Therefore, we determined the effects of baicalin, and berberine on the LPS-inducible NO and PGE2 accumulation in RAW264.7 cells. Baicalin treatment (3 and 10 μM) markedly inhibited NO and PGE2 productions induced by LPS (Figures 8(a) and 8(b)). On the other hand, 3 and 10 μM treatment of berberine failed to decrease in the NO induction, and, significantly, but less potently than baicalin, blocked PGE2 accumulation (Figures 8(a) and 8(b)).

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