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Methyl Protodioscin from the Roots of Asparagus cochinchinensis Attenuates Airway Inflammation by Inhibiting Cytokine Production.

Lee JH, Lim HJ, Lee CW, Son KH, Son JK, Lee SK, Kim HP - Evid Based Complement Alternat Med (2015)

Bottom Line: This downregulating effect of proinflammatory cytokine production was found to be mediated, at least in part, via inhibition of c-Jun N-terminal kinase (JNK) and c-Jun activation pathway.When examined on an in vivo model of airway inflammation in mice, lipopolysaccharide- (LPS-) induced acute lung injury, ACE, and MP significantly inhibited cell infiltration in the bronchoalveolar lavage fluid by the oral treatment at doses of 100-400 mg/kg and 30-60 mg/kg, respectively.All of these findings provide scientific evidence supporting the role of A. cochinchinensis as a herbal remedy in treating airway inflammation and also suggest a therapeutic value of MP on airway inflammatory disorders.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Kangwon National University, Chuncheon 200-701, Republic of Korea.

ABSTRACT
The present study was designed to find pharmacologically active compound against airway inflammation from the roots of Asparagus cochinchinensis. The 70% ethanol extract of the roots of A. cochinchinensis (ACE) was found to inhibit IL-6 production from IL-1β-treated lung epithelial cells (A549) and the major constituent, methyl protodioscin (MP), also strongly inhibited the production of IL-6, IL-8, and tumor necrosis factor- (TNF-) α from A549 cells at 10-100 μM. This downregulating effect of proinflammatory cytokine production was found to be mediated, at least in part, via inhibition of c-Jun N-terminal kinase (JNK) and c-Jun activation pathway. When examined on an in vivo model of airway inflammation in mice, lipopolysaccharide- (LPS-) induced acute lung injury, ACE, and MP significantly inhibited cell infiltration in the bronchoalveolar lavage fluid by the oral treatment at doses of 100-400 mg/kg and 30-60 mg/kg, respectively. MP also inhibited the production of proinflammatory cytokines such as IL-6, TNF-α, and IL-1β in lung tissue. All of these findings provide scientific evidence supporting the role of A. cochinchinensis as a herbal remedy in treating airway inflammation and also suggest a therapeutic value of MP on airway inflammatory disorders.

No MeSH data available.


Related in: MedlinePlus

Inhibition of methyl protodioscin (MP) on LPS-induced airway inflammation in mice. (a) Effects on the cell numbers in BALF; LPS was administered to mice intranasally. Total cell numbers in the BALF were counted using haemocytometer. The BALF was obtained at 16 h after LPS treatment. DEX: dexamethasone; FACS was used to differentiate between each cell type of inflammation-related cells. (b) Effects on proinflammatory cytokine generation. All cytokine levels were examined using real-time RT-PCR analysis of the lung tissue. For TNF-α measurement, the lung tissue of the mice sacrificed at 4 h after LPS treatment was used while the lung tissue at 16 h after LPS treatment was used for measuring the levels of IL-1β and IL-6. (c) Histological observation of lung tissues (H&E staining) and quantitative analysis of alveolar wall area (426 × 426 pixels). Here is represented one sample from five sets stained. ×100 (scale bar: 100 μm). Thickened alveolar wall and narrowed alveolar space were noted in the LPS-treated lung tissue (▼). Alveolar wall areas were quantitatively measured by ImageJ (NIH). +P < 0.1, ∗P < 0.05, and ∗∗P < 0.01, significantly different from the LPS-treated group (n = 5).
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fig6: Inhibition of methyl protodioscin (MP) on LPS-induced airway inflammation in mice. (a) Effects on the cell numbers in BALF; LPS was administered to mice intranasally. Total cell numbers in the BALF were counted using haemocytometer. The BALF was obtained at 16 h after LPS treatment. DEX: dexamethasone; FACS was used to differentiate between each cell type of inflammation-related cells. (b) Effects on proinflammatory cytokine generation. All cytokine levels were examined using real-time RT-PCR analysis of the lung tissue. For TNF-α measurement, the lung tissue of the mice sacrificed at 4 h after LPS treatment was used while the lung tissue at 16 h after LPS treatment was used for measuring the levels of IL-1β and IL-6. (c) Histological observation of lung tissues (H&E staining) and quantitative analysis of alveolar wall area (426 × 426 pixels). Here is represented one sample from five sets stained. ×100 (scale bar: 100 μm). Thickened alveolar wall and narrowed alveolar space were noted in the LPS-treated lung tissue (▼). Alveolar wall areas were quantitatively measured by ImageJ (NIH). +P < 0.1, ∗P < 0.05, and ∗∗P < 0.01, significantly different from the LPS-treated group (n = 5).

Mentions: Based on these results, MP was pharmacologically evaluated in the same animal model. LPS treatment of mice induces inflammatory cell recruitment and detachment of the resident cells in the BALF, elevated levels of proinflammatory cytokines, and histological changes in the lung tissue. The total cells in BALF greatly increased (approximately sixfold) at 16 h after LPS treatment. FACS analysis provided differential cell counts. The numbers of infiltrated neutrophils, infiltrated and detached resident macrophages, and dendritic cells were greatly increased in the LPS-treated lung (Figure 6(a)). When the expression levels of proinflammatory molecules were measured, all of the mRNA concentrations of TNF-α (4 h), IL-1β (16 h), and IL-6 (16 h) in the lung tissue drastically increased as revealed by RT-PCR analysis (Figure 6(b)). In addition, the prominent hyperplasia of the alveolar cell layer and narrowed alveolar space was found in the LPS-treated lung tissues by histological comparison (Figure 6(c)).


Methyl Protodioscin from the Roots of Asparagus cochinchinensis Attenuates Airway Inflammation by Inhibiting Cytokine Production.

Lee JH, Lim HJ, Lee CW, Son KH, Son JK, Lee SK, Kim HP - Evid Based Complement Alternat Med (2015)

Inhibition of methyl protodioscin (MP) on LPS-induced airway inflammation in mice. (a) Effects on the cell numbers in BALF; LPS was administered to mice intranasally. Total cell numbers in the BALF were counted using haemocytometer. The BALF was obtained at 16 h after LPS treatment. DEX: dexamethasone; FACS was used to differentiate between each cell type of inflammation-related cells. (b) Effects on proinflammatory cytokine generation. All cytokine levels were examined using real-time RT-PCR analysis of the lung tissue. For TNF-α measurement, the lung tissue of the mice sacrificed at 4 h after LPS treatment was used while the lung tissue at 16 h after LPS treatment was used for measuring the levels of IL-1β and IL-6. (c) Histological observation of lung tissues (H&E staining) and quantitative analysis of alveolar wall area (426 × 426 pixels). Here is represented one sample from five sets stained. ×100 (scale bar: 100 μm). Thickened alveolar wall and narrowed alveolar space were noted in the LPS-treated lung tissue (▼). Alveolar wall areas were quantitatively measured by ImageJ (NIH). +P < 0.1, ∗P < 0.05, and ∗∗P < 0.01, significantly different from the LPS-treated group (n = 5).
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig6: Inhibition of methyl protodioscin (MP) on LPS-induced airway inflammation in mice. (a) Effects on the cell numbers in BALF; LPS was administered to mice intranasally. Total cell numbers in the BALF were counted using haemocytometer. The BALF was obtained at 16 h after LPS treatment. DEX: dexamethasone; FACS was used to differentiate between each cell type of inflammation-related cells. (b) Effects on proinflammatory cytokine generation. All cytokine levels were examined using real-time RT-PCR analysis of the lung tissue. For TNF-α measurement, the lung tissue of the mice sacrificed at 4 h after LPS treatment was used while the lung tissue at 16 h after LPS treatment was used for measuring the levels of IL-1β and IL-6. (c) Histological observation of lung tissues (H&E staining) and quantitative analysis of alveolar wall area (426 × 426 pixels). Here is represented one sample from five sets stained. ×100 (scale bar: 100 μm). Thickened alveolar wall and narrowed alveolar space were noted in the LPS-treated lung tissue (▼). Alveolar wall areas were quantitatively measured by ImageJ (NIH). +P < 0.1, ∗P < 0.05, and ∗∗P < 0.01, significantly different from the LPS-treated group (n = 5).
Mentions: Based on these results, MP was pharmacologically evaluated in the same animal model. LPS treatment of mice induces inflammatory cell recruitment and detachment of the resident cells in the BALF, elevated levels of proinflammatory cytokines, and histological changes in the lung tissue. The total cells in BALF greatly increased (approximately sixfold) at 16 h after LPS treatment. FACS analysis provided differential cell counts. The numbers of infiltrated neutrophils, infiltrated and detached resident macrophages, and dendritic cells were greatly increased in the LPS-treated lung (Figure 6(a)). When the expression levels of proinflammatory molecules were measured, all of the mRNA concentrations of TNF-α (4 h), IL-1β (16 h), and IL-6 (16 h) in the lung tissue drastically increased as revealed by RT-PCR analysis (Figure 6(b)). In addition, the prominent hyperplasia of the alveolar cell layer and narrowed alveolar space was found in the LPS-treated lung tissues by histological comparison (Figure 6(c)).

Bottom Line: This downregulating effect of proinflammatory cytokine production was found to be mediated, at least in part, via inhibition of c-Jun N-terminal kinase (JNK) and c-Jun activation pathway.When examined on an in vivo model of airway inflammation in mice, lipopolysaccharide- (LPS-) induced acute lung injury, ACE, and MP significantly inhibited cell infiltration in the bronchoalveolar lavage fluid by the oral treatment at doses of 100-400 mg/kg and 30-60 mg/kg, respectively.All of these findings provide scientific evidence supporting the role of A. cochinchinensis as a herbal remedy in treating airway inflammation and also suggest a therapeutic value of MP on airway inflammatory disorders.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Kangwon National University, Chuncheon 200-701, Republic of Korea.

ABSTRACT
The present study was designed to find pharmacologically active compound against airway inflammation from the roots of Asparagus cochinchinensis. The 70% ethanol extract of the roots of A. cochinchinensis (ACE) was found to inhibit IL-6 production from IL-1β-treated lung epithelial cells (A549) and the major constituent, methyl protodioscin (MP), also strongly inhibited the production of IL-6, IL-8, and tumor necrosis factor- (TNF-) α from A549 cells at 10-100 μM. This downregulating effect of proinflammatory cytokine production was found to be mediated, at least in part, via inhibition of c-Jun N-terminal kinase (JNK) and c-Jun activation pathway. When examined on an in vivo model of airway inflammation in mice, lipopolysaccharide- (LPS-) induced acute lung injury, ACE, and MP significantly inhibited cell infiltration in the bronchoalveolar lavage fluid by the oral treatment at doses of 100-400 mg/kg and 30-60 mg/kg, respectively. MP also inhibited the production of proinflammatory cytokines such as IL-6, TNF-α, and IL-1β in lung tissue. All of these findings provide scientific evidence supporting the role of A. cochinchinensis as a herbal remedy in treating airway inflammation and also suggest a therapeutic value of MP on airway inflammatory disorders.

No MeSH data available.


Related in: MedlinePlus