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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.

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Effects of LFXY on the expression of TLR4 and NF-κB p65 in the lung tissue by western blot assay. The expression of NF-κB p65 (a) and TLR4 (b). 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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fig7: Effects of LFXY on the expression of TLR4 and NF-κB p65 in the lung tissue by western blot assay. The expression of NF-κB p65 (a) and TLR4 (b). Data presented were mean ± SEM. #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.

Mentions: TLR4/NF-κB signaling pathway induces the production of most proinflammatory cytokines including TNF-α, IL-1β, and IL-6, thus playing an important role in the pathogenesis of ALI. Western blot analysis was performed to determine the phosphorylation of NF-κB p65 and the expression of TLR4. As shown in Figure 7, LPS administration significantly increased the phosphorylation of NF-κB p65 in the lung, as compared with the sham group. However, pretreatment with LFXY (25, 50, and 100 mg/kg) inhibited the phosphorylation of NF-κB p65 in a dose-dependent manner. In addition, the expression of TLR4 was also observed to be significantly increased in the LPS-treated mice, while the tendency was dramatically attenuated by pretreatment with LFXY (25, 50, and 100 mg/kg). These results show that LFXY pretreatment could block the TLR4/NF-κB signaling pathway in a mouse model of LPS-induced 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
Effects of LFXY on the expression of TLR4 and NF-κB p65 in the lung tissue by western blot assay. The expression of NF-κB p65 (a) and TLR4 (b). 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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fig7: Effects of LFXY on the expression of TLR4 and NF-κB p65 in the lung tissue by western blot assay. The expression of NF-κB p65 (a) and TLR4 (b). Data presented were mean ± SEM. #P < 0.01 versus sham group; ∗P < 0.05 and ∗∗P < 0.01 versus LPS group.
Mentions: TLR4/NF-κB signaling pathway induces the production of most proinflammatory cytokines including TNF-α, IL-1β, and IL-6, thus playing an important role in the pathogenesis of ALI. Western blot analysis was performed to determine the phosphorylation of NF-κB p65 and the expression of TLR4. As shown in Figure 7, LPS administration significantly increased the phosphorylation of NF-κB p65 in the lung, as compared with the sham group. However, pretreatment with LFXY (25, 50, and 100 mg/kg) inhibited the phosphorylation of NF-κB p65 in a dose-dependent manner. In addition, the expression of TLR4 was also observed to be significantly increased in the LPS-treated mice, while the tendency was dramatically attenuated by pretreatment with LFXY (25, 50, and 100 mg/kg). These results show that LFXY pretreatment could block the TLR4/NF-κB signaling pathway in a mouse model of LPS-induced 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-&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