The anti-neuroinflammatory effects of dehydromiltirone and related mechanisms
10.3969/j.issn.1001-1978.2016.02.007
- VernacularTitle:去氢丹参新酮对神经炎症的抑制作用及机制研究
- Author:
Dechuan LI
;
Xiuqi BAO
;
Dewu ZHANG
;
Hua SUN
;
Jungui DAI
;
Dan ZHANG
- Publication Type:Journal Article
- Keywords:
dehydromiltirone;
neuroinflammation;
mi-croglia;
NF-κB;
PI3 K/Akt;
lipopolysaccharide
- From:
Chinese Pharmacological Bulletin
2016;(2):177-183
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the anti-neuroinflam-matory activities of dehydromiltirone and the underlying mechanisms in LPS-stimulated microglial cell line BV2 cells. Methods BV2 cells were pre-treated with de-hydromiltirone, then stimulated by LPS. The levels of nitric oxide( NO) were measured by Griess assay, and the concentrations of pro-inflammatory cytokines were measured by ELISA assay. Confocal fluorescence mi-croscopy was used to measure the expression of MAC-1, the biomarker of activated BV2 cells. The levels of-inducible nitric oxide synthase ( iNOS ) , cyclooxygen-ase-2 ( COX-2 ) , NF-κB and PI3 K/Akt were deter-mined by Western blot analysis. Results The treat-ment of dehydromiltirone significantly inhibited the pro-duction of NO, TNF-α and IL-6, attenuated the ex-pression of iNOS and COX-2 protein, and dampened the microglial activation in LPS-stimulated BV2 cells. The mechanistic study revealed that dehydromiltirone inhibited the phosphorylation of PI3 K and Akt in LPS-stimulated BV2 cells, and decreased NF-κB activation by suppressing the degradation of IκB. Conclusion dehydromiltirone shows significant anti-neuroinflamma-tory effects through inhibiting PI3 K/Akt phosphoryla-tion and then inhibiting NF-κB signaling pathway.
