Astragalin attenuates lipopolysaccharide-induced inflammatory responses by down-regulating NF-κB signaling pathway
Autor: | Lanxiang Jiang, Xiao Chu, Haihua Feng, Miaomiao Wei, Xuming Deng, Meixia Huo, Faya Martin Millimouno, Youssouf Sidime, Na Chen, Lanan Wassy Soromou |
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Rok vydání: | 2012 |
Předmět: |
Lipopolysaccharides
Male Lipopolysaccharide medicine.medical_treatment Flavonoid Acute Lung Injury Biophysics Down-Regulation Lung injury Pharmacology Biochemistry chemistry.chemical_compound Mice Pneumonia Bacterial Medicine Animals Kaempferols Molecular Biology chemistry.chemical_classification Mice Inbred BALB C business.industry Therapeutic effect Anti-Inflammatory Agents Non-Steroidal NF-kappa B Cell Biology In vitro Endotoxemia Disease Models Animal Cytokine chemistry Immunology Tumor necrosis factor alpha Astragalin business Signal Transduction |
Zdroj: | Biochemical and biophysical research communications. 419(2) |
ISSN: | 1090-2104 |
Popis: | Astragalin (AG), a flavonoid from many traditional herbs and medicinal plants, has been described to exhibit in vitro anti-inflammatory activity. The present study aimed to determine the protective effects and the underlying mechanisms of astragalin on lipopolysaccharide-induced endotoxemia and lung injury in mice. Mice were injected intraperitoneally (i.p.) with lipopolysaccharide (LPS) (dose range: 5–40 mg/kg). We observed mice on mortality for 7 days twice a day and recorded survival rates. In drug testing, we examined the therapeutic effects of astragalin (25, 50 or 75 mg/kg) on LPS- induced endotoxemia by dosing orally astragalin 1 hour before LPS challenge. Using an experimental model of LPS-induced acute lung injury (ALI), we examined the effect of astragalin in resolving lung injury. The investigations revealed that pretreatment with astragalin can improve survival during lethal endotoxemia and attenuate inflammatory responses in a murine model of lipopolysaccharide-induced acute lung injury. The mechanisms by which Astragalin exerts its anti-inflammatory effect are correlated with inhibition of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6) production via inactivation of NF-κB. |
Databáze: | OpenAIRE |
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