Home>>Signaling Pathways>> Immunology/Inflammation>> Apoptosis>>Naphthazarin

Naphthazarin Sale

(Synonyms: 萘茜,DHNQ; 5,8-Dihydroxy-1,4-naphthoquinone) 目录号 : GC60264

Naphthazarin(DHNQ)是天然存在的化合物,通过多种细胞机制有效,包括氧化应激,线粒体凋亡诱导因子(AIF)活化,微管解聚,干扰溶酶体功能和p53依赖性p21活化。Naphthazarin触发细胞凋亡(apoptosis)并具有抗肿瘤作用。

Naphthazarin Chemical Structure

Cas No.:475-38-7

规格 价格 库存 购买数量
100mg
¥675.00
现货
250mg
¥1,170.00
现货

电话:400-920-5774 Email: sales@glpbio.cn

Customer Reviews

Based on customer reviews.

Sample solution is provided at 25 µL, 10mM.

产品文档

Quality Control & SDS

View current batch:

产品描述

Naphthazarin (DHNQ) is a naturally occurring compound. Naphthazarin is effective by various cellular mechanisms including oxidative stress, activation of mitochondrial apoptosis-inducing factor (AIF), depolymerization of microtubules, interference with lysosomal function and p53-dependent p21 activation. Naphthazarin triggers apoptosis and has anti-tumor effects[1][2].

[1]. Seon Young Choi, et al. Naphthazarin has a protective effect on the 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine-induced Parkinson's disease model. J Neurosci Res. 2012 Sep;90(9):1842-9. [2]. Omar Aljanadi, et al. Stimulation of Suicidal Erythrocyte Death by Naphthazarin. Basic Clin Pharmacol Toxicol. 2015 Dec;117(6):369-74.

Chemical Properties

Cas No. 475-38-7 SDF
别名 萘茜,DHNQ; 5,8-Dihydroxy-1,4-naphthoquinone
Canonical SMILES O=C1C=CC(C2=C1C(O)=CC=C2O)=O
分子式 C10H6O4 分子量 190.15
溶解度 储存条件 Store at RT
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。
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。

溶解性数据

制备储备液
1 mg 5 mg 10 mg
1 mM 5.259 mL 26.295 mL 52.5901 mL
5 mM 1.0518 mL 5.259 mL 10.518 mL
10 mM 0.5259 mL 2.6295 mL 5.259 mL
  • 摩尔浓度计算器

  • 稀释计算器

  • 分子量计算器

质量
=
浓度
x
体积
x
分子量
 
 
 
*在配置溶液时,请务必参考产品标签上、MSDS / COA(可在Glpbio的产品页面获得)批次特异的分子量使用本工具。

计算

动物体内配方计算器 (澄清溶液)

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
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

Research Update

Pharmacological properties and derivatives of shikonin-A review in recent years

Pharmacol Res 2019 Nov;149:104463.PMID:31553936DOI:10.1016/j.phrs.2019.104463.

Shikonin is the major bioactive component extracted from the roots of Lithospermum erythrorhizon which is also known as "Zicao" in Traditional Chinese Medicine (TCM). Recent studies have shown that shikonin demonstrates various bioactivities related to the treatment of cancer, inflammation, and wound healing. This review aimed to provide an updated summary of recent studies on shikonin. Firstly, many studies have demonstrated that shikonin exerts strong anticancer effects on various types of cancer by inhibiting cell proliferation and migration, inducing apoptosis, autophagy, and necroptosis. Shikonin also triggers Reactive Oxygen Species (ROS) generation, suppressing exosome release, and activate anti-tumor immunity in multiple molecular mechanisms. Examples of these effects include modulating the PI3K/AKT/mTOR and MAPKs signaling; inhibiting the activation of TrxR1, PKM2, RIP1/3, Src, and FAK; and regulating the expression of ERP57, MMPs, ATF2, C-MYC, miR-128, and GRP78 (Bip). Next, the anti-inflammatory and wound-healing properties of shikonin were also reviewed. Furthermore, several studies focusing on shikonin derivatives were reviewed, and these showed that, with modification to the Naphthazarin ring or side chain, some shikonin derivatives display stronger anticancer activity and lower toxicity than shikonin itself. Our findings suggest that shikonin and its derivatives could serve as potential novel drug for the treatment of cancer and inflammation.

Naphthazarin has a protective effect on the 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine-induced Parkinson's disease model

J Neurosci Res 2012 Sep;90(9):1842-9.PMID:22513651DOI:10.1002/jnr.23061.

"Neurohormesis" refers to a response to a moderate level of stress that enhances the ability of the nervous systems to resist more severe stress that might be lethal or cause dysfunction or disease. Neurohormetic phytochemicals, such as, resveratrol, sulforaphane, curcumin, and catechins, protect neurons against injury and disease. Naphthoquinones, such as, juglone and plumbagin, induce robust hormetic stress responses. However, the possibility that subtoxic dose of 5,8-dihydroxy-1,4-naphthoquinone (Naphthazarin) may protect against brain diseases via the activation of an adaptive stress response pathway in the brain has not been investigated. In this study, we examined the neurohormetic effect of a subtoxic dose of Naphthazarin in a Parkinson's disease model. It was found that, under these conditions, Naphthazarin enhanced movement ability, prevented loss of dopaminergic neurons, and attenuated neuroinflammation in a 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine-induced Parkinson's disease model. Furthermore, it was found that the neuroprotective effect of Naphthazarin was mediated by the suppression of astroglial activation in response to 1-methyl-4-phenylpyridine treatment. In conclusion, we suggest that Naphthazarin, in view of its hormetic effect on neuroprotection, be viewed as a potential treatment for Parkinson's disease and other neurodegenerative diseases associated with neuroinflammation.

The microtubule depolymerizing agent Naphthazarin induces both apoptosis and autophagy in A549 lung cancer cells

Apoptosis 2011 Sep;16(9):924-39.PMID:21667044DOI:10.1007/s10495-011-0613-1.

Naphthazarin (DHNQ, 5,8-dihydroxy-l,4-naphthoquinone) is a naturally available 1,4-naphthoquinone derivatives. In this study, we focused on elucidating the cytotoxic mechanism of Naphthazarin in A549 non-small cell lung carcinoma cells. Naphthazarin reduced the A549 cell viability considerably with an IC(50) of 16.4 ± 1.6 μM. Naphthazarin induced cell death in a dose- and time-dependent manner by activating apoptosis and autophagy pathways. Specifically, we found Naphthazarin inhibited the PI3K/Akt cell survival signalling pathway, measured by p53 and caspase-3 activation, and PARP cleavage. It also resulted in an increase in the ratio of Bax/Bcl2 protein levels, indicating activation of the mitochondrial apoptotic pathway. Similarly Naphthazarin triggered LC3II expression and induced autophagic flux in A549 cells. We demonstrated further that Naphthazarin is a microtubule inhibitor in cell-free system and in A549 cells. Naphthazarin treatment depolymerized interphase microtubules and disorganised spindle microtubules and the majority of cells arrested at the G(2)/M transition. Together, these data suggest that Naphthazarin, a microtubule depolymerizer which activates dual cell death machineries, could be a potential novel chemotherapeutic agent.

Stimulation of Suicidal Erythrocyte Death by Naphthazarin

Basic Clin Pharmacol Toxicol 2015 Dec;117(6):369-74.PMID:26013059DOI:10.1111/bcpt.12420.

The 1,4-naphthoquinone derivative Naphthazarin may trigger apoptosis and is thus considered for the treatment of malignancy. On the other hand, Naphthazarin decreases neurotoxicity. In analogy to apoptosis of nucleated cells, erythrocytes may enter eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by cell membrane scrambling with translocation of phosphatidylserine to the erythrocyte surface. Signalling leading to triggering of eryptosis include increase in cytosolic Ca(2+)-activity ([Ca(2+)]i), ceramide and oxidative stress. The present study explored whether Naphthazarin impacts on eryptosis and, if so, to unravel underlying mechanisms. To this end, erythrocyte volume was estimated from forward scatter, phosphatidylserine abundance at the erythrocyte surface from FITC-annexin-V-binding, [Ca(2+)]i from Fluo3 fluorescence, reactive oxidant species (ROS) from 2',7'-dichlorodihydrofluorescein diacetate (DCFDA) fluorescence and ceramide abundance at the erythrocyte surface from binding of fluorescent antibodies in flow cytometry. As a result, a 24-hr exposure of human erythrocytes to Naphthazarin (10 μM) significantly decreased erythrocyte forward scatter, significantly increased the percentage of annexin-V-binding cells, significantly increased ceramide abundance at the erythrocyte surface and significantly increased ROS. The effect of Naphthazarin on annexin-V-binding was not significantly blunted by removal of extracellular Ca(2+). In conclusion, Naphthazarin stimulates eryptosis, an effect at least in part due to oxidative stress and enhanced ceramide abundance at the erythrocyte surface.

Naphthazarin protects against glutamate-induced neuronal death via activation of the Nrf2/ARE pathway

Biochem Biophys Res Commun 2013 Apr 19;433(4):602-6.PMID:23537652DOI:10.1016/j.bbrc.2013.03.041.

Nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway is an important cellular stress response pathway involved in neuroprotection. We previously screened several natural phytochemicals and identified plumbagin as a novel activator of the Nrf2/ARE pathway that can protect neurons against ischemic injury. Here we extended our studies to natural and synthetic derivatives of plumbagin. We found that 5,8-dimethoxy-1,4-naphthoquinone (Naphthazarin) is a potent activator of the Nrf2/ARE pathway, up-regulates the expression of Nrf2-driven genes in primary neuronal and glial cultures, and protects neurons against glutamate-induced excitotoxicity.