Deoxyshikonin
(Synonyms: 去氧紫草素) 目录号 : GC38767
Deoxyshikonin 是从 Lithospermum erythrorhizon Sieb 中分离得到的，具有抗肿瘤活性。
Cas No.:43043-74-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Deoxyshikonin is isolated from Lithospermum erythrorhizon Sieb with antitumor activity. Deoxyshikonin increases the expression of VEGF-C and VEGF-A mRNA in HMVEC-dLy, promotes HIF-1α and HIF-1β subunit interaction and binds to specific DNA sequences targeted by HIF, indicates a prolymphangiogenesis as well as a proangiogenesis effect in vitro[1]. Deoxyshikonin shows significant synergic antimicrobial activity against S. pneumonia (MIC=17 μg/mL), also shows significantly inhibitory activities against MRSA[2].
[1]. Prangsaengtong O, et al. Enhancement of Lymphangiogenesis In Vitro via the Regulations of HIF-1α Expression and Nuclear Translocation by Deoxyshikonin. Evid Based Complement Alternat Med. 2013;2013:148297. [2]. Zhang S, et al. Antibacterial effects of Traditional Chinese Medicine monomers against Streptococcus pneumoniae via inhibiting pneumococcal histidine kinase (VicK). Front Microbiol. 2015 May 20;6:479.
| Cas No. | 43043-74-9 | SDF | |
| 别名 | 去氧紫草素 | ||
| Canonical SMILES | O=C1C(CC/C=C(C)/C)=CC(C2=C1C(O)=CC=C2O)=O | ||
| 分子式 | C16H16O4 | 分子量 | 272.3 |
| 溶解度 | DMSO : 33.33 mg/mL (122.40 mM; ultrasonic and warming and heat to 60°C) | 储存条件 | 4°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.6724 mL | 18.3621 mL | 36.7242 mL |
| 5 mM | 0.7345 mL | 3.6724 mL | 7.3448 mL |
| 10 mM | 0.3672 mL | 1.8362 mL | 3.6724 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Deoxyshikonin reversibly inhibits cytochrome P450 2B6
Biopharm Drug Dispos 2020 Apr;41(4-5):221-225.PMID:32364297DOI:10.1002/bdd.2230.
Deoxyshikonin, a natural shikonin derivative, is the major component of Lithospermum erythrorhizon and exhibits various pharmacological effects such as lymphangiogenetic, antibacterial, wound healing, and anticancer effects. To investigate the herb-drug interaction potential associated with Deoxyshikonin, the inhibitory effects of Deoxyshikonin on eight major cytochrome P450 (CYP) enzymes were examined using cocktail substrate-incubated human liver microsomes. Deoxyshikonin strongly inhibited CYP2B6-catalyzed bupropion hydroxylation, with a Ki value of 3.5 μM, and the inhibition was confirmed using purified human CYP2B6. The inhibition was reversible because the inhibitory effect of Deoxyshikonin was not dependent on the preincubation time. The results indicated that deoxyshikonin-induced drug-drug interaction should be considered when any herb containing Deoxyshikonin is used for conventional medications.
Deoxyshikonin inhibits cisplatin resistance of non-small-cell lung cancer cells by repressing Akt-mediated ABCB1 expression and function
J Biochem Mol Toxicol 2020 Oct;34(10):e22560.PMID:32627280DOI:10.1002/jbt.22560.
Drug resistance is a large challenge for the treatment of non-small-cell lung cancer (NSCLC). Deoxyshikonin is the naphthoquinol compound with anticancer activity. However, the role and mechanism of Deoxyshikonin in cisplatin resistance of NSCLC remain poorly understood. Cell viability was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. Cell apoptosis was evaluated by flow cytometry and caspase-3 activity. We found that cisplatin-resistant A549/cis and H1299/cis cells had higher cisplatin resistance than A549 and H1299 cells, respectively. Deoxyshikonin contributed to cisplatin-induced viability inhibition and apoptosis in A549/cis and H1299/cis cells. Moreover, Deoxyshikonin inhibited phosphorylation of Akt and the expression and function of ATP-binding cassette subfamily B member 1 (ABCB1). Activation of protein kinase B (Akt) pathway attenuated the effect of Deoxyshikonin on cisplatin resistance and ABCB1 expression and function in A549/cis and H1299/cis cells. In conclusion, Deoxyshikonin suppressed cisplatin resistance in cisplatin-resistant NSCLC cells by repressing Akt signaling-mediated ABCB1 expression.
Deoxyshikonin Inhibits Viability and Glycolysis by Suppressing the Akt/mTOR Pathway in Acute Myeloid Leukemia Cells
Front Oncol 2020 Aug 7;10:1253.PMID:32850379DOI:10.3389/fonc.2020.01253.
Deoxyshikonin was reported to exhibit an anti-tumor effect in colorectal cancer. However, no studies are available to illustrate the effect of Deoxyshikonin on acute myeloid leukemia (AML). The effects of Deoxyshikonin on viability, apoptosis, caspase-3/7 activity, and cytochrome (Cyt) C expression were evaluated by Cell Counting Kit-8 assay, flow cytometry analysis, caspase-3/7 activity assay, and western blot analysis, respectively. Glucose consumption and lactate production were measured to determine the glycolysis level. The expression of pyruvate kinase M2 (PKM2) was detected by quantitative real-time polymerase chain reaction and western blot analysis. The results showed that Deoxyshikonin inhibited cell viability and increased the apoptotic rate, the caspase-3/7 activity, and the Cyt C protein level in AML cells in a dose-dependent manner. Additionally, Deoxyshikonin concentration-dependently decreased glucose consumption, lactate production, and PKM2 expression in AML cells. Deoxyshikonin inactivated the protein kinase B (Akt)/mammalian target of the rapamycin (mTOR) pathway. The activation of the Akt/mTOR pathway reversed the effects of Deoxyshikonin on viability, apoptosis, and glycolysis in AML cells. In conclusion, Deoxyshikonin dampened the viability and the glycolysis of AML cells by suppressing PKM2 via inactivation of the Akt/mTOR signaling.
Deoxyshikonin isolated from Arnebia euchroma inhibits colorectal cancer by down-regulating the PI3K/Akt/mTOR pathway
Pharm Biol 2019 Dec;57(1):412-423.PMID:31230505DOI:10.1080/13880209.2019.1626447.
Context: Shikonins, a series of natural occurring naphthoquinones extracted from Arnebia euchroma (Royle) Jonst. (Boraginaceae), have antitumor activities and low toxicity. Objective: To illuminate potential activity and mechanism of shikonins against colorectal cancer (CRC). Materials and methods: Five shikonins were isolated from A. euchroma, and elucidated by extensive spectroscopic analysis. Anti-proliferative activities of shikonins (0-100 μg/mL) on human colorectal cells were evaluated by MTT and CCK-8 for 24 or 48 h. Cell apoptosis and cycle distribution were examined by FCM analysis. The expression of PI3K/Akt/mTOR pathway mRNAs and proteins was analysed by RT-PCR and Western blot, respectively. Cell viability, cell apoptosis, cell cycle and protein expression were measured, when co-treated with PI3K/Akt/mTOR pathway inhibitors. The in vivo activity of Deoxyshikonin was evaluated using xenograft tumour model. Results: Deoxyshikonin and another four shikonins were isolated and identified. Deoxyshikonin exhibited anti-proliferative activity with IC50 of 10.97 μM against HT29 cells. Moreover, the percentage of early apoptotic cells and G0/G1 cells increased from 1 to 29% and 44 to 67% with 0-50 μg/mL Deoxyshikonin, respectively. Deoxyshikonin also down-regulated the expression of PI3K, p-PI3K, Akt, p-Akt308 and mTOR proteins in HT29 and DLD-1 cells. Moreover, LY294002, NVP-BEZ235 and MK-2206 can make Deoxyshikonin more cell proliferation inhibited, cell cycle arrested at G0/G1 and apoptosis promoted. In vivo study, the weight of tumour tissues at Deoxyshikonin groups was significantly reduced compared with the control group, and PI3K, p-PI3K, Akt, p-Akt308 and mTOR expression was decreased. Discussion and conclusions: We can conclude that Deoxyshikonin isolated from Arnebia euchroma inhibited CRC through the PI3K/Akt/mTOR pathway.
Deoxyshikonin Mediates Heme Oxygenase-1 Induction and Apoptotic Response via p38 Signaling in Tongue Cancer Cell Lines
Int J Mol Sci 2022 Jun 26;23(13):7115.PMID:35806120DOI:10.3390/ijms23137115.
Deoxyshikonin (DSK), a phytochemical constituent, has been documented to elicit various oncostatic properties alone or in combination with established therapeutics. However, its role in restraining oral squamous cell carcinoma (OSCC) is mostly unclear. Here, we examined the tumor-suppressive effect of DSK and explored the molecular mechanisms underlying DSK's activities on controlling oral cancer. Our results showed that DSK dose-dependently lessened the cell viability of tongue cancer cell lines, involving induction of cell cycle arrest at the sub-G1 phase and apoptotic cell death. Moreover, a unique signature of apoptosis-related proteins, including augmented nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) expression and caspase activation, was observed in DSK-treated tongue cancer cell lines. Furthermore, DSK-mediated upregulation of HO-1 and cleavage of caspase-9 and -3 were significantly inhibited by pharmacological blockage of p38 kinase. Collectively, these data revealed that DSK halted cell cycle progression and elicited cell apoptosis in tongue cancer cell lines, reshaping a p38-dependent profile of apoptotic proteome. Our findings provided novel insights into the therapeutic implications of a natural compound on the management of OSCC.