Yellow crystalline powder
Albizia julibrissin,Lobelia chinensis,Ginkgo biloba,Hedyotis diffusa,Calophyllum membranaceum
amentoflavone/Didemethyl-ginkgetin/4H-1-Benzopyran-4-one, 8-[5-(5,7-dihydroxy-4-oxo-4H-1-benzopyran-2-yl)-2-hydroxyphenyl]-5,7-dihydroxy-2-(4-hydroxyphenyl)/4H-1-Benzopyran-4-one, 8-[5-(5,7-dihydroxy-4-oxo-4H-1-benzopyran-2-yl)-2-hydroxyphenyl]-5,7-dihydroxy-2-(4-hydroxyphenyl)-/8-[5-(5,7-Dihydroxy-4-oxo-4H-chromen-2-yl)-2-hydroxyphenyl]-5,7-dihydroxy-2-(4-hydroxyphenyl)-4H-chromen-4-one/Didemethylginkgetin/Tridemethylsciadopitysin/4H-1-Benzopyran-4-one, 8-(5-(5,7-dihydroxy-4-oxo-4H-1-benzopyran-2-yl)-2-hydroxyphenyl)-5,7-dihydroxy-2-(4-hydroxyphenyl)-
910.5±65.0 °C at 760 mmHg
HS Code Reference
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For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:1617-53-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Objective: Amentoflavone is the main component of Selaginella tamariscina widely known as an oriental traditional medicinal stuff that has been known to have a variety of medicinal effects such as the induction of apoptosis, antimetastasis, and anti-inflammation. However, the effect of amentoflavone on autophagy has not been reported until now. The aim of this study was to investigate whether amentoflavone has a positive effect on the induction of autophagy related to cell aging.
Materials and methods: In this experimental study, the aging of young cells was induced by the treatment with insulinlike growth factor-1 (IGF-1) at 50 ng/mL three times every two days. The effect of amentoflavone on the cell viability was evaluated in A549 and WI-38 cells using 3-(4,5-dimethyl-2-yl)-2,5- diphenyl tetrazolium bromide (MTT) assay. The induction of autophagy was detected using autophagy detection kit. The expression of proteins related to autophagy and IGF-1 signaling pathway was examined by western blot analysis and immunofluorescence assay.
Results: First of all, it was found that amentoflavone induces the formation of autophagosome. In addition, it enhanced the expression level of Atg7 and increased the expression levels of Beclin1, Atg3, and LC3 associated with the induction of autophagy in immunofluorescence staining and western blot analyses. Moreover, amentoflavone inhibited the cell aging induced by IGF-1 and hydrogen peroxide. In particular, the levels of p53 and p-p21 proteins were increased in the presence of amentoflavone. Furthermore, amentoflavone increased the level of SIRT1 deacetylating p53.
Conclusion: Our results suggest that amentoflavone could play a positive role in the inhibition of various diseases associated with autophagy and the modulation of p53.
Aging; Amentoflavone; SIRT1; p53.
Amentoflavone Induces Autophagy and Modulates p53
Hye-Jung Park 1 , Moon-Moo Kim 2
Streptococcus suis, an important zoonotic pathogen, has caused considerable economic losses in the swine industry and severe public health issues worldwide. The development of a novel effective strategy for the prevention and therapy of S. suis is urgently needed. Here, amentoflavone, a natural biﬂavonoid compound isolated from Chinese herbs that has negligible anti-S. suis activity, was identified as a potent antagonist of suilysin (SLY)-mediated hemolysis without interfering with the expression of SLY. Amentoflavone effectively inhibited SLY oligomerization, which is critical for its pore-forming activity. The treatment with amentoflavone reduced S. suis-induced cytotoxicity in macrophages (J774 cells). Furthermore, S. suis-infected mice that received amentoflavone exhibited lower mortality and bacterial burden. Additionally, amentoflavone significantly decreased the production of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and IL-6 in an S. suis-infected cell model. Analyses of signaling pathways demonstrated that amentoflavone reduced S. suis-induced inflammation in S. suis serotype 2 (SS2)-infected cells by regulating the p38, Jun N-terminal protein kinase 1 and 2 (JNK1/2), and NF-κB pathways. The antivirulence and anti-inflammatory properties of amentoflavone against S. suis infection provide the possibility for future pharmaceutical application of amentoflavone in the treatment of S. suis infection.IMPORTANCE The widespread use of antibiotics in therapy and in the prevention of Streptococcus suis infection in the swine industry raises concerns for the emergence of a resistant strain. The use of antivirulence agents has potential benefits, mainly because of the reduced selective pressure for the development of bacterial resistance. In this study, we found that amentoflavone is an effective agent against S. suis serotype 2 (SS2) infection both in vitro and in vivo Our results demonstrated that amentoflavone is a promising anti-infective therapeutic for S. suis infections, due to its antivirulence and anti-inflammatory effects without antibacterial activity, with fewer side effects than conventional antibacterial agents.
Aging; Amentoflavone; SIRT1; p53.
Amentoflavone Ameliorates Streptococcus suis-Induced Infection In Vitro and In Vivo
Xue Shen # 1 2 , Xiaodi Niu # 1 2 , Gen Li 2 , Xuming Deng 3 2 , Jianfeng Wang 3 2
2018 Nov 30
Background/aim: A previous study indicated that amentoflavone inhibits tumor growth of breast cancer. However, the anti-cancer effects and mechanism of amentoflavone in hepatocellular carcinoma (HCC) have not been elucidated. The aim of the present study was to verify the effect of amentoflavone on tumor progression in HCC.
Materials and methods: HCC SK-Hep1 cells were treated with different concentrations of amentoflavone or 10 μM PD98059 (extracellular signal-regulated kinases (ERK) inhibitor) for 48 h, respectively, and then cell viability, NF-κB activation, levels of tumor progression-associated proteins, and cell invasion were evaluated with 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), NF-κB reporter gene assay, western blotting, and cell invasion assay.
Results: The results demonstrated that both amentoflavone and PD98059 not only significantly reduced cell viability, NF-κB activation, and cell invasion, but also inhibited the expression of tumor progression-associated proteins. In addition, we found that amentoflavone suppresses ERK phosphorylation.
Conclusion: The results of the present study suggest that amentoflavone down-regulates ERK-modulated tumor progression in HCC.
Amentoflavone; ERK; NF-κB; hepatocellular carcinoma.
Amentoflavone Inhibits ERK-modulated Tumor Progression in Hepatocellular Carcinoma In Vitro
Kun-Ching Lee 1 2 , Jai-Jen Tsai 3 , Chih-Wei Tseng 4 , Yu-Cheng Kuo 5 6 , Yao-Chen Chuang 7 , Song-Shei Lin 8 , Fei-Ting Hsu 9 10 11