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Protective Effects of Li-Fei-Xiao-Yan Prescription on Lipopolysaccharide-Induced Acute Lung Injury via Inhibition of Oxidative Stress and the TLR4/NF- κ B Pathway

View Article: PubMed Central - PubMed

ABSTRACT

Li-Fei-Xiao-Yan prescription (LFXY) has been clinically used in China to treat inflammatory and infectious diseases including inflammatory lung diseases. The present study was aimed at evaluating the potential therapeutic effects and potential mechanisms of LFXY in a murine model of lipopolysaccharide- (LPS-) induced acute lung injury (ALI). In this study, the mice were orally pretreated with LFXY or dexamethasone (positive drug) before the intratracheal instillation of LPS. Our data indicated that pretreatment with LFXY enhanced the survival rate of ALI mice, reversed pulmonary edema and permeability, improved LPS-induced lung histopathology impairment, suppressed the excessive inflammatory responses via decreasing the expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and chemokine (MIP-2) and inhibiting inflammatory cells migration, and repressed oxidative stress through the inhibition of MPO and MDA contents and the upregulation of antioxidants (SOD and GSH) activities. Mechanistically, treatment with LFXY significantly prevented LPS-induced TLR4 expression and NF-κB (p65) phosphorylation. Overall, the present study suggests that LFXY protected mice from acute lung injury induced by LPS via inhibition of TLR4/NF-κB p65 activation and upregulation of antioxidative enzymes and it may be a potential preventive and therapeutic agent for ALI in the clinical setting.

No MeSH data available.


Related in: MedlinePlus

Effects of LFXY on the production of TNF-α, IL-6, IL-1β, and MIP-2 in BALF. BALF was collected 24 h after LPS challenge and the concentrations of TNF-α (a), IL-6 (b), IL-1β (c), and MIP-2 (d) in BALF were determined. Data presented were mean ± SEM. #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.
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fig6: Effects of LFXY on the production of TNF-α, IL-6, IL-1β, and MIP-2 in BALF. BALF was collected 24 h after LPS challenge and the concentrations of TNF-α (a), IL-6 (b), IL-1β (c), and MIP-2 (d) in BALF were determined. Data presented were mean ± SEM. #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.

Mentions: The effects of LFXY on TNF-α, IL-6, IL-1β, and MIP-2 concentrations in BALF were analyzed by ELISA 6 h after LPS stimulation. As shown in Figure 6, the concentrations of TNF-α, IL-6, IL-1β, and MIP-2 in BALF were obviously elevated in the LPS group compared with those in the sham group. However, pretreatment with LFXY reversed the levels of TNF-α, IL-6, IL-1β, and MIP-2 (P < 0.05 or P < 0.01). DEX was also shown to exert a significant inhibitory effect on the production of these cytokines and chemokines in BALF (P < 0.01).


Protective Effects of Li-Fei-Xiao-Yan Prescription on Lipopolysaccharide-Induced Acute Lung Injury via Inhibition of Oxidative Stress and the TLR4/NF- κ B Pathway
Effects of LFXY on the production of TNF-α, IL-6, IL-1β, and MIP-2 in BALF. BALF was collected 24 h after LPS challenge and the concentrations of TNF-α (a), IL-6 (b), IL-1β (c), and MIP-2 (d) in BALF were determined. Data presented were mean ± SEM. #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.
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Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC5382312&req=5

fig6: Effects of LFXY on the production of TNF-α, IL-6, IL-1β, and MIP-2 in BALF. BALF was collected 24 h after LPS challenge and the concentrations of TNF-α (a), IL-6 (b), IL-1β (c), and MIP-2 (d) in BALF were determined. Data presented were mean ± SEM. #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.
Mentions: The effects of LFXY on TNF-α, IL-6, IL-1β, and MIP-2 concentrations in BALF were analyzed by ELISA 6 h after LPS stimulation. As shown in Figure 6, the concentrations of TNF-α, IL-6, IL-1β, and MIP-2 in BALF were obviously elevated in the LPS group compared with those in the sham group. However, pretreatment with LFXY reversed the levels of TNF-α, IL-6, IL-1β, and MIP-2 (P < 0.05 or P < 0.01). DEX was also shown to exert a significant inhibitory effect on the production of these cytokines and chemokines in BALF (P < 0.01).

View Article: PubMed Central - PubMed

ABSTRACT

Li-Fei-Xiao-Yan prescription (LFXY) has been clinically used in China to treat inflammatory and infectious diseases including inflammatory lung diseases. The present study was aimed at evaluating the potential therapeutic effects and potential mechanisms of LFXY in a murine model of lipopolysaccharide- (LPS-) induced acute lung injury (ALI). In this study, the mice were orally pretreated with LFXY or dexamethasone (positive drug) before the intratracheal instillation of LPS. Our data indicated that pretreatment with LFXY enhanced the survival rate of ALI mice, reversed pulmonary edema and permeability, improved LPS-induced lung histopathology impairment, suppressed the excessive inflammatory responses via decreasing the expression of proinflammatory cytokines (TNF-&alpha;, IL-1&beta;, and IL-6) and chemokine (MIP-2) and inhibiting inflammatory cells migration, and repressed oxidative stress through the inhibition of MPO and MDA contents and the upregulation of antioxidants (SOD and GSH) activities. Mechanistically, treatment with LFXY significantly prevented LPS-induced TLR4 expression and NF-&kappa;B (p65) phosphorylation. Overall, the present study suggests that LFXY protected mice from acute lung injury induced by LPS via inhibition of TLR4/NF-&kappa;B p65 activation and upregulation of antioxidative enzymes and it may be a potential preventive and therapeutic agent for ALI in the clinical setting.

No MeSH data available.


Related in: MedlinePlus