| In vitro: |
| J Asian Nat Prod Res. 2014;16(8):865-75. | | Polygalasaponin F inhibits secretion of inflammatory cytokines via NF-κB pathway regulation.[Pubmed: 25082394] | To study the anti-neuroinflammatory mechanisms of polygalasaponin F (PS-F), ELISA method was used to detect the secretion of inflammatory cytokines.
METHODS AND RESULTS:
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.
CONCLUSIONS:
PS-F inhibits the secretions of neuroinflammatory cytokines by the regulation of NF-κB-signaling pathway. | | J Asian Nat Prod Res. 2014 Jan;16(1):59-69. | | Polygalasaponin F against rotenone-induced apoptosis in PC12 cells via mitochondria protection pathway.Polygalasaponin F against rotenone-induced apoptosis in PC12 cells via mitochondria protection pathway.[Pubmed: 24382325] | To investigate the protective effect and the underlying mechanism of Polygalasaponin F (PS-F) against rotenone-induced PC12 cells, the cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay.
METHODS AND RESULTS:
The cell apoptosis rate was analyzed using flow cytometry. The reactive oxygen species was examined using 2',7'-dichlorofluorescin diacetate, and the adenosine triphosphate depletion was examined using a luciferase-coupled quantification assay. JC-1 staining was used to detect the mitochondrial membrane potential. Western blotting analysis was used to determine cytochrome c, p53, Bax, Bcl-2, and caspase-3. Treatment of PC12 cells with rotenone (1-10 μmol/l) significantly reduced the cell viability in a concentration-dependent manner. Treatment with Polygalasaponin F (0.1, 1, and 10 μmol/l) increased the viability of rotenone-induced PC12 cells, decreased rotenone-induced apoptosis, restored rotenone-induced mitochondrial dysfunction, and suppressed rotenone-induced protein expression. Polygalasaponin F showed a dose-dependent manner in all the treatments. Polygalasaponin F protects PC12 cells against rotenone-induced apoptosis via ameliorating the mitochondrial dysfunction.
CONCLUSIONS:
Thus, Polygalasaponin F may be a potential bioactive compound for the treatment of Parkinson's disease. |
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