Apocynin - CAS 498-02-2
Catalog number: 498-02-2
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C9H10O3
Molecular Weight:
166.17
COA:
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Targets:
Others
Description:
Apocynin, also known as acetovanillone, is a natural organic compound structurally related to vanillin. It has been isolated from a variety of plant sources and is being studied for its variety of pharmacological properties.Apocynin is a selective NADPH-oxidase inhibitor with IC50 of 10 μM.
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Purity:
>98%
Synonyms:
Acetovanillone
MSDS:
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1.Parthenolide and DMAPT exert cytotoxic effects on breast cancer stem-like cells by inducing oxidative stress, mitochondrial dysfunction and necrosis.
Carlisi D1, Buttitta G2, Di Fiore R2, Scerri C3, Drago-Ferrante R2, Vento R2,4, Tesoriere G1,4. Cell Death Dis. 2016 Apr 14;7:e2194. doi: 10.1038/cddis.2016.94.
Triple-negative breast cancers (TNBCs) are aggressive forms of breast carcinoma associated with a high rate of recidivism. In this paper, we report the production of mammospheres from three lines of TNBC cells and demonstrate that both parthenolide (PN) and its soluble analog dimethylaminoparthenolide (DMAPT) suppressed this production and induced cytotoxic effects in breast cancer stem-like cells, derived from dissociation of mammospheres. In particular, the drugs exerted a remarkable inhibitory effect on viability of stem-like cells. Such an effect was suppressed by N-acetylcysteine, suggesting a role of reactive oxygen species (ROS) generation in the cytotoxic effect. Instead z-VAD, a general inhibitor of caspase activity, was ineffective. Analysis of ROS generation, performed using fluorescent probes, showed that both the drugs stimulated in the first hours of treatment a very high production of hydrogen peroxide. This event was, at least in part, a consequence of activation of NADPH oxidases (NOXs), as it was reduced by apocynin and diphenylene iodinium, two inhibitors of NOXs.
2.[Mechanisms for inhibitory effect of ALDH2 on doxorubicin-induced cytotoxicity in C2C12 myogenic cell line].
Gao Y1, Zhu S2, Xu Y2, Li Y1, Zhou S3, Liu X1. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2016 Mar 28;41(3):264-71. doi: 10.11817/j.issn.1672-7347.2016.03.007.
in English, Chinese目的:探讨乙醛脱氢酶2(aldehyde dehydrogenase 2,ALDH2)对多柔吡星(doxorubicin,DOX)所致肌原细胞毒性的保护作用及其机制。方法:以小鼠C2C12肌原细胞为研究对象,通过基因转染方式调节细胞内ALDH2表达水平,以流式细胞术检测细胞凋亡率,MTT法检测细胞增殖抑制率,化学荧光法检测组织活性氧(reactive oxygen species,ROS)、4羟壬烯醛(4-hydroxynonenal,4-HNE)蛋白加合物含量及caspase-3/7活性,Western印迹检测Bcl-2,NADPH氧化酶2(NADPH oxidase 2,NOX2)、胞浆调节亚单位p-p47PHOX水平。结果:ALDH2过表达可显著降低DOX所致C2C12细胞凋亡及增殖抑制,而抑制ALDH2的表达则增加DOX对C2C12细胞凋亡诱导及增殖抑制作用;ALDH2过表达可下调p47PHOX磷酸化水平,抑制NOX2活化及ROS生成,而ALDH2低表达则上调p47PHOX磷酸化水平,促进NOX2活化及ROS生成;此外,NOX2活性抑制剂apocynin可抑制p47PHOX磷酸化、ROS生成及caspase-3/7的酶活性,同时增加 ALDH2酶活性及其mRNA水平。结论:DOX所致的肌原细胞毒性与NOX2依赖性细胞氧化应激增强、ALDH2酶活性及表达降低有关,而ALDH2通过抑制上述NOX2信号,减轻细胞凋亡而发挥保护细胞作用。.
3.Reactive oxygen species are involved in insulin-dependent regulation of autophagy in primary rat podocytes.
Audzeyenka I1, Rogacka D2, Piwkowska A2, Rychlowski M3, Bierla JB4, Czarnowska E4, Angielski S2, Jankowski M5. Int J Biochem Cell Biol. 2016 Mar 26;75:23-33. doi: 10.1016/j.biocel.2016.03.015. [Epub ahead of print]
Autophagy is an intracellular defense mechanism responsible for the turnover of damaged or non-functional cellular constituents. This process provides cells with energy and essential compounds under unfavorable environmental conditions-such as oxidative stress and hyperglycemia, which are both observed in diabetes. The most common diabetes complication is diabetic nephropathy (DN), which can lead to renal failure. This condition often includes impaired podocyte function. Here we investigated autophagic activity in rat podocytes cultured with a high insulin concentration (300nM). Autophagy was activated after 60min of insulin stimulation. Moreover, this effect was abolished following pharmacological (apocynin) or genetic (siRNA) inhibition of NAD(P)H oxidase activity, indicating that insulin-dependent autophagy stimulation involved reactive oxygen species (ROS). We also observed a continuous and time-dependent increase of podocyte albumin permeability in response to insulin, and this process was slightly improved by autophagy inhibition following short-term insulin exposure.
4.Sphingosine 1-Phosphate-Induced ICAM-1 Expression via NADPH Oxidase/ROS-Dependent NF-κB Cascade on Human Pulmonary Alveolar Epithelial Cells.
Lin CC1, Yang CC2, Cho RL3, Wang CY1, Hsiao LD1, Yang CM4. Front Pharmacol. 2016 Mar 31;7:80. doi: 10.3389/fphar.2016.00080. eCollection 2016.
The intercellular adhesion molecule-1 (ICAM-1) expression is frequently correlated with the lung inflammation. In lung injury, sphingosine-1-phosphate (S1P, bioactive sphingolipid metabolite), participate gene regulation of adhesion molecule in inflammation progression and aggravate tissue damage. To investigate the transduction mechanisms of the S1P in pulmonary epithelium, we demonstrated that exposure of HPAEpiCs (human pulmonary alveolar epithelial cells) to S1P significantly induces ICAM-1 expression leading to increase monocyte adhesion on the surface of HPAEpiCs. These phenomena were effectively attenuated by pretreatments with series of inhibitors such as Rottlerin (PKCδ), PF431396 (PYK2), diphenyleneiodonium chloride (DPI), apocynin (NADPH oxidase), Edaravone (ROS), and Bay11-7082 (NF-κB). Consistently, knockdown with siRNA transfection of PKCδ, PYK2, p47 (phox) , and p65 exhibited the same results. Pretreatment with both Gq-coupled receptor antagonist (GPA2A) and Gi/o-coupled receptor antagonist (GPA2) also blocked the upregulation of ICAM-1 protein and mRNA induced by S1P.
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CAS 498-02-2 Apocynin

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