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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.


Schemes of the mechanism for the protective effect of LFXY on LPS-induced ALI. The shaded parts indicate the molecules affected by LFXY.
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fig8: Schemes of the mechanism for the protective effect of LFXY on LPS-induced ALI. The shaded parts indicate the molecules affected by LFXY.

Mentions: This study demonstrates that LFXY could attenuate LPS-induced lung injury. The protective effect of LFXY is shown to result from inhibiting inflammatory response and oxidative stress and is also associated with the downregulation of TLR4/NF-κB signaling pathway (Figure 8). Thus, our findings suggested that LFXY might act as a potential therapeutic agent for treatment of ALI.


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
Schemes of the mechanism for the protective effect of LFXY on LPS-induced ALI. The shaded parts indicate the molecules affected by LFXY.
© Copyright Policy
Related In: Results  -  Collection

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

fig8: Schemes of the mechanism for the protective effect of LFXY on LPS-induced ALI. The shaded parts indicate the molecules affected by LFXY.
Mentions: This study demonstrates that LFXY could attenuate LPS-induced lung injury. The protective effect of LFXY is shown to result from inhibiting inflammatory response and oxidative stress and is also associated with the downregulation of TLR4/NF-κB signaling pathway (Figure 8). Thus, our findings suggested that LFXY might act as a potential therapeutic agent for treatment of ALI.

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.