|Source:||The roots of Lithosperraum erythrorhizon Sieb. et Zucc.|
|Biological Activity or Inhibitors:||1. Acetylshikonin (ASK), a derivate of shikonin, can effectively inhibit tumor cells.
2. Acetylshikonin can be used to treat hepatocellular carcinoma cells expressing hepatitis B virus X protein (HBX) by inducing ER stress , an oncoprotein from hepatitis B virus.
3. Acetylshikonin exhibits the most potent antiapoptosis activity through the inhibition of the generation of reactive oxygen species as well as protection of the loss of mitochondria membrane potential.
4. Acetylshikonin inhibits the production of eicosanoid, is due to the attenuation of cytosolic phospholipase A(2) membrane recruitment via the decrease in [Ca(2+)](i) and to the blockade of cyclooxygenase and 5-lipoxygenase activity.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||3.0273 mL||15.1364 mL||30.2728 mL||60.5455 mL||75.6819 mL|
|5 mM||0.6055 mL||3.0273 mL||6.0546 mL||12.1091 mL||15.1364 mL|
|10 mM||0.3027 mL||1.5136 mL||3.0273 mL||6.0546 mL||7.5682 mL|
|50 mM||0.0605 mL||0.3027 mL||0.6055 mL||1.2109 mL||1.5136 mL|
|100 mM||0.0303 mL||0.1514 mL||0.3027 mL||0.6055 mL||0.7568 mL|
Eur J Pharmacol. 2014 Jul 15;735:132-40.
|Acetylshikonin induces apoptosis of hepatitis B virus X protein-expressing human hepatocellular carcinoma cells via endoplasmic reticulum stress.[Pubmed: 24769509]|
|When Acetylshikonin was added to Hep3B cells stably expressing HBX, it induced apoptosis in a dose-dependent manner. Acetylshikonin induced upregulation and export of Nur77 to the cytoplasm and activation of JNK. Likewise, suppression of Nur77 and JNK inactivation protected the cells from Acetylshikonin-induced apoptosis, indicating that Nur77 upregulation and JNK activation were required for Acetylshikonin-mediated apoptosis. Furthermore, Acetylshikonin increased the expression of Bip and ubiquitination levels of cellular proteins, features of endoplasmic reticulum (ER) stress, via the production of reactive oxygen species in a dose-dependent manner. Suppression of reactive oxygen species with N-acetylcysteine reduced levels of Bip protein and ubiquitination levels of cellular proteins during Acetylshikonintreatment, leading to protection of cells from apoptosis. Cycloheximide treatment reduced Acetylshikonin-induced ER stress, suggesting that protein synthesis is involved in Acetylshikonin-induced ER stress. Moreover, we showed using salubrinal, an ER stress inhibitor that reactive oxygen species production, Acetylshikonin activation, and Nur77 upregulation and its translocation to cytoplasm are necessary for ER-induced stress. Interestingly, we found that JNK inactivation suppresses Acetylshikonin-induced ER stress, whereas Nur77 siRNA treatment does not, indicating that JNK is required for Acetylshikonin-induced ER stress. Accordingly, we report that Acetylshikonin induces ER stress, which is prerequisite for apoptosis of HBX-expressing hepatocellular carcinoma cells.|
AAPS PharmSciTech. 2014 Apr;15(2):425-33.
|Encapsulation of acetylshikonin by polyamidoamine dendrimers for preparing prominent nanoparticles.[Pubmed: 24449188]|
|Acetylshikonin (AS) has demonstrated antitumor potential. However, the development of therapeutic applications utilizing Acetylshikonin is inhibited by its poor solubility in water. In the present work, polyamidoamine (PAMAM) dendrimers and their PEGylated derivatives were employed to increase the solubility of Acetylshikonin. A distinct color transition was observed during the encapsulation of Acetylshikonin suggesting strong intermolecular forces between PAMAM and Acetylshikonin. Ultraviolet-visible, high-performance liquid chromatography, and (1)H NMR were used to verify the interaction between PAMAM and Acetylshikonin. The maximum amount of combined Acetylshikonin to each PAMAM molecule was determined. The cytotoxicity of Acetylshikonin nanoparticles was evaluated against leukemia (K562) and breast cancer (SK-BR-3) cell lines; the Acetylshikonin nanoparticles were shown to effectively inhibit tumor cells.|
Evid Based Complement Alternat Med. 2013;2013:937370.
|Acetylshikonin, a Novel AChE Inhibitor, Inhibits Apoptosis via Upregulation of Heme Oxygenase-1 Expression in SH-SY5Y Cells.[Pubmed: 24302971]|
|We have identified twelve phytochemicals (emodin, aloe-emodin, chrysophanol, and rhein in Rhei Radix Et Rhizoma; xanthotoxin, phellopterin, alloisoimperatorin, and imperatorin in Angelicae dahuricae Radix; shikonin, Acetylshikonin, isovalerylshikonin, and β,β-dimethylacrylshikonin in Arnebiae Radix) as candidates of AChEIs that were not previously reported in the literature. In addition to AChEI activity, a series of cell-based experiments were conducted for the investigation of their neuroprotective activities. We found that Acetylshikonin and its derivatives prevented apoptotic cell death induced by hydrogen peroxide in human and rat neuronal SH-SY5Y and PC12 cells at 10 μM. We showed that Acetylshikonin exhibited the most potent antiapoptosis activity through the inhibition of the generation of reactive oxygen species as well as protection of the loss of mitochondria membrane potential. Furthermore, we identified for the first time that the upregulation of heme oxygenase 1 by Acetylshikonin is a key step mediating its antiapoptotic activity from oxidative stress in SH-SY5Y cells.|
World J Gastroenterol. 2009 Apr 21;15(15):1816-20.
|Inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 in vitro and in vivo.[Pubmed: 19370777]|
|AIM: To investigate the inhibitory effect of Acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS: MTT assay was used to assess the inhibitory effect of Acetylshikonin on proliferation of SGC-7901 cells.Antitumor effect of Acetylshikonin on a mouse SGC-7901 model was also determined. RESULTS: Forty-eight hours after treatment with Acetylshikonin, MTT assay showed that Acetylshikonin inhibited the proliferation of SGC-7901 cells in a dose-dependent manner. The half maximal inhibitory concentration of Acetylshikonin to SGC-7901 cells was 0.428 +/- 0.07 mg/L. Cell shrinkage, nuclear pyknosis and chromatin condensation, which are the characteristics of cell apoptosis, were observed in treated SGC-7901 cells and the percentage of apoptosis increased in a dose-dependent manner. Acetylshikonin down-regulated the expression of Bcl-2 and up-regulated the expression of Bax in the treated SGC-7901 cells compared with the controls. The experiment in vivo showed that 0.5, 1, and 2 mg/kg of Acetylshikonin significantly inhibited the growth of tumor in the mouse SGC-7901 model, with an inhibitory rate of 25.00%-55.76%. CONCLUSION: Acetylshikonin inhibits the growth of SGC-7901 cells in vitro and in vivo by inducing cell apoptosis.|
Eur J Pharmacol. 2009 Apr 1;607(1-3):234-43.
|The influence of acetylshikonin, a natural naphthoquinone, on the production of leukotriene B4 and thromboxane A2 in rat neutrophils.[Pubmed: 19232341]|
|Acetylshikonin alone stimulated extracellular signal regulated kinase (ERK) phosphorylation and enhanced this response in cells stimulated with A23187 and fMLP. The phosphorylation of ERKs and cytosolic phospholipase A(2) was attenuated by U0126, a mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor. Acetylshikonin facilitated both A23187- and fMLP-mediated translocation of 5-lipoxygenase to the membrane. Acetylshikonin attenuated both fMLP- and ionomycin-mediated [Ca(2+)](i) elevation. These results indicate that the inhibition of eicosanoid production by Acetylshikonin is due to the attenuation of cytosolic phospholipase A(2) membrane recruitment via the decrease in [Ca(2+)](i) and to the blockade of cyclooxygenase and 5-lipoxygenase activity.|