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01.06.2014 | Original Research Paper | Ausgabe 6/2014

Inflammation Research 6/2014

p-Synephrine suppresses lipopolysaccharide-induced acute lung injury by inhibition of the NF-κB signaling pathway

Zeitschrift:
Inflammation Research > Ausgabe 6/2014
Autoren:
Qianchao Wu, Ruisheng Li, Lanan Wassy Soromou, Na Chen, Xue Yuan, Guoquan Sun, Beibei Li, Haihua Feng
Wichtige Hinweise
Q. Wu and R. Li contributed equally to this work.

Abstract

Objective

We investigated whether p-synephrine exerts potent anti-inflammatory effects against acute lung injury (ALI) induced by lipopolysaccharide (LPS) in vivo, and we further investigated the inhibitory mechanism of p-synephrine in LPS-induced ALI.

Methods

Lipopolysaccharide (0.5 mg/kg) was instilled intranasally in phosphate-buffered saline to induce acute lung injury, and 6, 24, and 48 h after LPS was given, bronchoalveolar lavage fluid was obtained to measure pro-inflammatory mediator. We also evaluated the effects of p-synephrine on LPS-induced the severity of pulmonary injury. The phosphorylation of nuclear factor-κB (NF-κB) p65 protein was analyzed by Western blotting.

Results

Our data showed that p-synephrine significantly reduced the amount of inflammatory cells, the lung wet-to-dry weight (W/D) ratio, reactive oxygen species, myeloperoxidase activity and enhanced superoxide dismutase (SOD) in mice with LPS-induced ALI. Tumor necrosis factor α and interleukin (IL)-6 concentrations decreased significantly while the concentration of IL-10 was significantly increased after p-synephrine pretreatment. In addition, p-synephrine suppressed not only the phosphorylation of NF-κB but also the degradation of its inhibitor (IκBα).

Conclusions

These results suggested that the inhibition of NF-κB activation and the regulation of SOD are involved in the mechanism of p-synephrine’s protection against ALI.

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