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p-Synephrine suppresses lipopolysaccharide-induced acute lung injury by inhibition of the NF-κB signaling pathway.
Inflamm Res 2014; 63(6):429-39IR

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.

Authors+Show Affiliations

Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24487736

Citation

Wu, Qianchao, et al. "P-Synephrine Suppresses Lipopolysaccharide-induced Acute Lung Injury By Inhibition of the NF-κB Signaling Pathway." Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.], vol. 63, no. 6, 2014, pp. 429-39.
Wu Q, Li R, Soromou LW, et al. P-Synephrine suppresses lipopolysaccharide-induced acute lung injury by inhibition of the NF-κB signaling pathway. Inflamm Res. 2014;63(6):429-39.
Wu, Q., Li, R., Soromou, L. W., Chen, N., Yuan, X., Sun, G., ... Feng, H. (2014). P-Synephrine suppresses lipopolysaccharide-induced acute lung injury by inhibition of the NF-κB signaling pathway. Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.], 63(6), pp. 429-39. doi:10.1007/s00011-014-0715-7.
Wu Q, et al. P-Synephrine Suppresses Lipopolysaccharide-induced Acute Lung Injury By Inhibition of the NF-κB Signaling Pathway. Inflamm Res. 2014;63(6):429-39. PubMed PMID: 24487736.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - p-Synephrine suppresses lipopolysaccharide-induced acute lung injury by inhibition of the NF-κB signaling pathway. AU - Wu,Qianchao, AU - Li,Ruisheng, AU - Soromou,Lanan Wassy, AU - Chen,Na, AU - Yuan,Xue, AU - Sun,Guoquan, AU - Li,Beibei, AU - Feng,Haihua, Y1 - 2014/02/01/ PY - 2013/06/05/received PY - 2014/01/22/accepted PY - 2013/12/06/revised PY - 2014/2/4/entrez PY - 2014/2/4/pubmed PY - 2015/1/28/medline SP - 429 EP - 39 JF - Inflammation research : official journal of the European Histamine Research Society ... [et al.] JO - Inflamm. Res. VL - 63 IS - 6 N2 - 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. SN - 1420-908X UR - https://www.unboundmedicine.com/medline/citation/24487736/p_Synephrine_suppresses_lipopolysaccharide_induced_acute_lung_injury_by_inhibition_of_the_NF_κB_signaling_pathway_ L2 - https://dx.doi.org/10.1007/s00011-014-0715-7 DB - PRIME DP - Unbound Medicine ER -