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Erschienen in: Inflammation Research 1/2016

01.01.2016 | Original Research Paper

Isorhamnetin protects mice from lipopolysaccharide-induced acute lung injury via the inhibition of inflammatory responses

verfasst von: Gefu Chi, Weiting Zhong, Yan Liu, Gejin Lu, Hongming Lü, Dacheng Wang, Fei Sun

Erschienen in: Inflammation Research | Ausgabe 1/2016

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Abstract

Objective and design

Isorhamnetin (Isor), a 3-O-methylated metabolite of quercetin, has shown antioxidant and anti-proliferative effects in previous studies. In this study, we investigated the anti-inflammatory effect of Isor on LPS-induced acute lung injury (ALI). Accordingly, we evaluated the effect of Isor on cytokine production elevated by LPS (1 μg/ml) in vitro. An in vivo ALI murine model was also established via lipopolysaccharide inhalation (LPS, 20 mg/kg), and the cytokine levels and inflammatory cell count in bronchoalveolar lavage fluid (BALF) were evaluated. The observed lung injury was assessed using histopathologic sections via H&E straining. Furthermore, to investigate whether the anti-inflammatory effect of Isor is associated with NF-κB and MAPKs pathway activation, the phosphorylated levels of ERK, JNK, IκBa and NF-κB(p65) were determined.

Results

Isor significantly inhibited LPS-induced TNF-α, IL-1β and IL-6 secretion both in vitro and in vivo. Neutrophil infiltration and edema in an ALI model were substantially alleviated. The histopathological changes induced by LPS were lessened by Isor. Additionally, Isor notably suppressed the phosphorylation of ERK, JNK, IκBa and NF-κB(p65) activated by LPS in vivo.

Conclusions

Isor showed efficient protective effects on an LPS-induced ALI model. MAPKs and NF-κB pathways are critical for Isor to perform its protective effects.
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Metadaten
Titel
Isorhamnetin protects mice from lipopolysaccharide-induced acute lung injury via the inhibition of inflammatory responses
verfasst von
Gefu Chi
Weiting Zhong
Yan Liu
Gejin Lu
Hongming Lü
Dacheng Wang
Fei Sun
Publikationsdatum
01.01.2016
Verlag
Springer International Publishing
Erschienen in
Inflammation Research / Ausgabe 1/2016
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-015-0887-9

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