| In vitro: |
| J Cell Biochem. 2011 Dec;112(12):3816-23. | | Ailanthoidol suppresses lipopolysaccharide-stimulated inflammatory reactions in RAW264.7 cells and endotoxin shock in mice.[Pubmed: 21826708] | The biological properties of ailanthoidol, a neolignan from Zanthoxylum ailanthoides or Salvia miltiorrhiza Bunge, which is used in Chinese traditional herbal medicine, have not been evaluated.
METHODS AND RESULTS:
Here, we report that ailanthoidol inhibits inflammatory reactions in macrophages and protects mice from endotoxin shock. Our in vitro experiments showed that ailanthoidol suppressed the generation of nitric oxide (NO) and prostaglandin E(2) , as well as the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 induced by lipopolysaccharide (LPS) in RAW264.7 cells. Similarly, ailanthoidol inhibited the production of inflammatory cytokines induced by LPS in RAW264.7 cells, including interleukin (IL)-1β and IL-6. In an animal model, ailanthoidol protected BALB/c mice from LPS-induced endotoxin shock, possibly through inhibition of the production of inflammatory cytokines and NO.
CONCLUSIONS:
Collectively, ailanthoidol inhibited the production of inflammatory mediators and may be a potential target for treatment of various inflammatory diseases. | | 대한의생명과학회지, 2014, 20:62-69. | | Anti-Adipogenic Activity of Ailanthoidol on 3T3-L1 Adipocytes.[Reference: WebLink] | Previous our study demonstrated that Ailanthoidol (3-deformylated 2-arylbenzo[b]furan), a neolignan from Zanthoxylum ailanthoides or Salvia miltiorrhiza Bunge, is a novel anti-inflammatory agent.
METHODS AND RESULTS:
In this investigation, we examined the anti-adipogenic effect of Ailanthoidol. Our data showed that Ailanthoidol suppressed lipid droplet formation and adipocyte differentiation in 3T3-L1 cells. Treatment of the 3T3-L1 adipocytes with Ailanthoidol resulted in an attenuation of the releases of leptin and interleukin-6. The expression of peroxisome proliferator-activated receptor (PPAR)γ and CCAAT/ enhancer-binding protein (C/EBP)α, the central transcriptional regulators of adipogenesis, was decreased by treatment with Ailanthoidol. Additionally, Ailanthoidol treatment increased the phosphorylation levels of 5" adenosine monophosphateactivated protein kinase.
CONCLUSIONS:
These results suggest that Ailanthoidol effectively suppresses adipogenesis and that it exerts its role mainly through the significant down-regulation of PPARγ and C/EBPα expression.
Our findings provide important insights into the mechanisms underlying the anti-adipogenic activity of Ailanthoidol. |
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