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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 LPS-induced mortality in ALI mice (a), the lung wet/dry ratio (b), and protein contents in BALF (c). Data represented the mean ± SEM (n = 10). #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.
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fig2: Effects of LFXY on LPS-induced mortality in ALI mice (a), the lung wet/dry ratio (b), and protein contents in BALF (c). Data represented the mean ± SEM (n = 10). #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.

Mentions: As shown in Figure 2(a), the accumulative mortality during 6 days in LPS group was significantly increased (90%, P < 0.01 versus sham group) compared with the sham group (the mortality of 0%). However, the accumulative mortality was significantly reduced after pretreatment with LFXY or dexamethasone (DEX). The mortalities of mice in LFXY groups (25, 50, and 100 mg/kg) were 60% (P < 0.05), 55% (P < 0.05), and 45% (P < 0.01), respectively, which were evidently lower as compared with those in LPS group (90%). It is suggested that pretreatment with LFXY could significantly protect the mice from LPS-induced death in a dose-dependent manner.


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 LPS-induced mortality in ALI mice (a), the lung wet/dry ratio (b), and protein contents in BALF (c). Data represented the mean ± SEM (n = 10). #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.
© Copyright Policy
Related In: Results  -  Collection

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

fig2: Effects of LFXY on LPS-induced mortality in ALI mice (a), the lung wet/dry ratio (b), and protein contents in BALF (c). Data represented the mean ± SEM (n = 10). #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.
Mentions: As shown in Figure 2(a), the accumulative mortality during 6 days in LPS group was significantly increased (90%, P < 0.01 versus sham group) compared with the sham group (the mortality of 0%). However, the accumulative mortality was significantly reduced after pretreatment with LFXY or dexamethasone (DEX). The mortalities of mice in LFXY groups (25, 50, and 100 mg/kg) were 60% (P < 0.05), 55% (P < 0.05), and 45% (P < 0.01), respectively, which were evidently lower as compared with those in LPS group (90%). It is suggested that pretreatment with LFXY could significantly protect the mice from LPS-induced death in a dose-dependent manner.

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