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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 carrageenan-induced paw edema formation by BSE. BSE was administered to rats at the oral dose of 0.3 or 1 g/kg/day. Then, paw edema was induced by subcutaneously injecting 1% solution of carrageenan dissolved in saline (0.1 mL per animal) into the hind paw. The thickness of the paw was measured before and 1–4 h after carrageenan injection. Dexamethasone (Dex, 1 mg/kg, p.o.) was used as a positive control. Data represents the mean ± S.E.M. of six animals (significant as compared with carrageenan alone, **P < 0.01). For data points where error bars could not be seen, the standard error was subtended by the data point. BSE: Bojesodok-eum.
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fig1: Inhibition of carrageenan-induced paw edema formation by BSE. BSE was administered to rats at the oral dose of 0.3 or 1 g/kg/day. Then, paw edema was induced by subcutaneously injecting 1% solution of carrageenan dissolved in saline (0.1 mL per animal) into the hind paw. The thickness of the paw was measured before and 1–4 h after carrageenan injection. Dexamethasone (Dex, 1 mg/kg, p.o.) was used as a positive control. Data represents the mean ± S.E.M. of six animals (significant as compared with carrageenan alone, **P < 0.01). For data points where error bars could not be seen, the standard error was subtended by the data point. BSE: Bojesodok-eum.

Mentions: First, we determined the inhibitory effects of BSE on acute inflammation in vivo. We used the carrageenan-induced paw edema model, which is one of the widely used models for screening the efficacy of anti-inflammatory drugs [24]. Paw edema formation by carrageenan was observed from 1 h and persisted up to 4 h after injection (Figure 1). Administrations of BSE (0.3 and 1 g/kg) significantly inhibited the ability of carrageenan to induce paw swelling. We also showed the inhibitory effect of dexamethasone, a positive control, on edema formation. In addition, we confirmed the effects of BSE on histological profiles of dorsum and ventrum pedis skin. The changes of histomorphometrical analysis of hind paw skins were listed in Table 2. Marked increases of skin thicknesses on both dorsum and ventrum pedis were detected by treatment of carrageenan, which was blocked by BSE treatments (Figure 2(a)). Moreover, iNOS and COX-2 are crucial enzymes in the pathological process of acute inflammation. We assessed the expression of iNOS and COX-2 in the paw by real-time PCR. BSE treatment significantly prevented the iNOS and COX-2 induction by carrageenan injection in rats (Figure 2(b)). These results suggest that BSE suppresses the acute phase of paw swelling in association with inflammation in vivo.


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 carrageenan-induced paw edema formation by BSE. BSE was administered to rats at the oral dose of 0.3 or 1 g/kg/day. Then, paw edema was induced by subcutaneously injecting 1% solution of carrageenan dissolved in saline (0.1 mL per animal) into the hind paw. The thickness of the paw was measured before and 1–4 h after carrageenan injection. Dexamethasone (Dex, 1 mg/kg, p.o.) was used as a positive control. Data represents the mean ± S.E.M. of six animals (significant as compared with carrageenan alone, **P < 0.01). For data points where error bars could not be seen, the standard error was subtended by the data point. BSE: Bojesodok-eum.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Inhibition of carrageenan-induced paw edema formation by BSE. BSE was administered to rats at the oral dose of 0.3 or 1 g/kg/day. Then, paw edema was induced by subcutaneously injecting 1% solution of carrageenan dissolved in saline (0.1 mL per animal) into the hind paw. The thickness of the paw was measured before and 1–4 h after carrageenan injection. Dexamethasone (Dex, 1 mg/kg, p.o.) was used as a positive control. Data represents the mean ± S.E.M. of six animals (significant as compared with carrageenan alone, **P < 0.01). For data points where error bars could not be seen, the standard error was subtended by the data point. BSE: Bojesodok-eum.
Mentions: First, we determined the inhibitory effects of BSE on acute inflammation in vivo. We used the carrageenan-induced paw edema model, which is one of the widely used models for screening the efficacy of anti-inflammatory drugs [24]. Paw edema formation by carrageenan was observed from 1 h and persisted up to 4 h after injection (Figure 1). Administrations of BSE (0.3 and 1 g/kg) significantly inhibited the ability of carrageenan to induce paw swelling. We also showed the inhibitory effect of dexamethasone, a positive control, on edema formation. In addition, we confirmed the effects of BSE on histological profiles of dorsum and ventrum pedis skin. The changes of histomorphometrical analysis of hind paw skins were listed in Table 2. Marked increases of skin thicknesses on both dorsum and ventrum pedis were detected by treatment of carrageenan, which was blocked by BSE treatments (Figure 2(a)). Moreover, iNOS and COX-2 are crucial enzymes in the pathological process of acute inflammation. We assessed the expression of iNOS and COX-2 in the paw by real-time PCR. BSE treatment significantly prevented the iNOS and COX-2 induction by carrageenan injection in rats (Figure 2(b)). These results suggest that BSE suppresses the acute phase of paw swelling in association with inflammation in vivo.

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