2. Academic Validation
  3. Polygalasaponin F inhibits secretion of inflammatory cytokines via NF-κB pathway regulation

Polygalasaponin F inhibits secretion of inflammatory cytokines via NF-κB pathway regulation

  • J Asian Nat Prod Res. 2014;16(8):865-75. doi: 10.1080/10286020.2014.918962.
Wei Wei 1,  Yu-He Yuan,  Yan-Na Gao,  Wen-Fen Yan,  Chuang-Jun Li,  Dong-Ming Zhang,  Nai-Hong Chen
Affiliations

Affiliation

  • 1 a State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study, Department of Pharmacology , Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College , Beijing 100050 , China.
PMID: 25082394 DOI: 10.1080/10286020.2014.918962
Abstract

To study the anti-neuroinflammatory mechanisms of polygalasaponin F (PS-F), ELISA method was used to detect the secretion of inflammatory cytokines. Western blot was used to detect the protein expression and phosphorylation levels. Immunofluorescence assay was used to observe the NF-κB nuclear translocation. PS-F could inhibit the release of inflammatory cytokines TNF-α and NO induced by lipopolysaccharides (LPS) and reduce the expression of inducible nitric oxide synthases (iNOS). As for MAPK-signaling pathway, PS-F could only inhibit the phosphorylation levels of p38 MAPK, but did not significantly affect the phosphorylation levels of JNK and ERK1/2 protein kinases. PS-F could inhibit NF-κB nuclear translocation in a dose-dependent manner. The results of Western blot assay were consistent with immunofluorescence assays. Meanwhile, p38-specific inhibitor SB203580 (20 μM) and p65-specific inhibitor PDTC (100 μM) were, respectively, administered as a positive control. In addition, PS-F could significantly inhibit the cytotoxicity of conditioned medium prepared by LPS-stimulated BV-2 microglia (LPS conditioned media) to neuronal PC12 cells and improve cell viability. PS-F inhibits the secretions of neuroinflammatory cytokines by the regulation of NF-κB-signaling pathway.

Keywords

NF-κB; neuroinflammation; p38; polygalasaponin F.

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