| CAS |
No.458-37-7 |
| 中文名称 |
姜黄素(10mM in DMSO,无菌） |
| 英文名称 |
Curcumin(10mM in DMSO，Sterile） |
| 分子式 |
C21H20O6 |
| 分子量 |
368.38 |
| 溶解性 |
请根据自己的实验要求使用。 |
| 外观(性状) |
无菌溶液 |
| 储存条件 |
Stroe at -20℃，6 months. |
| 靶点 |
P300/CREB;HAT;Keap1-Nrf2 |
| 通路 |
Epigenetics;NF-κB |
| 背景说明 |
Curcumin是乙酰转移酶 p300/CREB 结合蛋白特异性抑制剂，抑制组蛋白/非组蛋白的乙酰化和组蛋白乙酰转移酶依赖的染色质转录。Curcumin 对 NF-κb 和 MAPKs 有抑制作用，并具有抗炎、抗氧化、抗血管生成等多种生理活性。 |
| 生物活性 |
Curcumin (Diferuloylmethane)， a natural phenolic compound， is a p300/CREB-binding protein-specific inhibitor of acetyltransferase， represses the acetylation of histone/nonhistone proteins and histone acetyltransferase-dependent chromatin transcription. Curcumin shows inhibitory effects on NF-κB and MAPKs， and has diverse pharmacologic effects including anti-inflammatory， antioxidant， antiproliferative and antiangiogenic activities. Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification.[1-8] |
| In Vitro |
Curcumin exerts its chemopreventive effects partly through the activation of nuclear factor (erythroid-2 related) factor 2 (Nrf2) and its antioxidant and phase II detoxifying enzymes[1]. Curcumin inhibits T47D cells growth， with IC50s of 25， 19 and 17.5 μM for 24， 48 and 72 h MTT assays respectively. IC50s of curcumin and silibinin mixture against T47D cells， are 17.5， 15， and 12 μM for 24， 48， and 72 h exposure times， respectively[2]. Curcumin (2.5-80 μM) induces apoptotic cell death in AGS and HT-29 cell lines， and the IC50 is 21.9±0.1， 40.7±0.5 μM， respectively， in both AGS and HT-29 cell lines. Curcumin-induced apoptosis requires caspase activities in AGS and HT-29 cells. Curcumin induces ER Ca2+ decline and mitochondrial Ca2+ overloading[3]. Curcumin induces the G2/M cell cycle arrest of LNCaP and PC-3 cells in a dose dependent manner. Curcumin upregulates the protein level of NF-kappaB inhibitor IkappaBalpha and downregulates protein levels of c-Jun and AR[5]. |
| In Vivo |
Curcumin (10 mg/kg， p.o.) significantly prevents decrease in the percentage of sucrose consumption， as compared to the CMS-exposed rats. Curcumin treatment results in significant prevention of increase in TNF-α and IL-6 levels in stressed rats[4]. Curcumin decreases binding of p300/CREB-binding protein (CBP) at the brain-derived neurotrophic factor (BDNF) promoter at 20 mg/kg (i.p.)， reduces binding of P300/CBP at the BDNF promoter at 40 mg/kg， and decreases binding all the four proteins of p300/CBP and H3K9ac/H4K5ac at the BDNF promoter at 60 mg/kg in chronic constriction injury (CCI) rats[6]. |
| 细胞实验 |
T47D breast cancer cell line is grown in RPMI 1640 supplemented with 10% FBS， 2 mg/mL sodium bicarbonate， 0.05 mg/mL penicillin G， 0.08 mg/mL streptomycin. Culture is maintained on plastic flask and incubated at 37°C in 5% CO2. After growing sufficient amount of cells， cytotoxic effect of silibinin and curcumin is studied by 24， 48 and 72 h MTT assays in which 1000 cell/well are cultivated in a 96 well plate. After 24 h incubation in 37°C with humidified atmosphere containing 5% CO2， the cells are treated with serial concentrations of curcumin (5， 10， 20， 30， 40， 50， 60， 80， 100 μM)， silibinin (20， 40， 60， 80， 100， 120， 140， 180， 200 μM)， and curcumin-silibinin mixture (each of them 5， 10， 20， 30， 40， 50， 60， 80， 100 μM) for 24， 48 and 72 h in the quadruplicate manner， in addition to cells with 200 μL culture medium containing 10% DMSO for control. After incubation， the medium of all wells of the plate are exchanged with fresh medium and the cells are leaved for 24 h in incubator. Then， medium of all wells are removed carefully and 50 μL of 2 mg/mL MTT dissolved in PBS is added to each wells and the plate is covered with aluminum foil and incubated for 4.5 h again. After removing content of the wells， 200 μL pure DMSO is added to the wells. Then， 25 μL Sorensen’s glycine buffer is added and immediately absorbance of each wells is read in 570 nm using EL×800 Microplate Absorbance Reader with reference wavelength of 630 nm.[2] |
| 动物实验 |
Curcumin (10?mg/kg)， freshly suspended in saline， is administrated by oral gavage once a day for 3?weeks. Forty rats are randomLy assigned to 4 groups (n=10/each group): group I receives saline and serves as control， group II receives curcumin， group III is exposed to CMS andreceive saline and group IV are subjected to CMS andreceive curcumin.[4] |
| 数据来源文献 |
[1]. Gao S， et al. Curcumin attenuates arsenic-induced hepatic injuries and oxidative stress in experimental mice through activation of Nrf2 pathway， promotion of arsenic methylation and urinary excretion. Food Chem Toxicol. 2013 Jul 18. pii: S0278-6915(13)004
[2]. Nasiri M， et al. Curcumin and Silibinin Inhibit Telomerase Expression in T47D Human Breast Cancer Cells. Asian Pac J Cancer Prev. 2013;14(6):3449-53.
[3]. Cao A， et all. Curcumin induces apoptosis in human gastric carcinoma AGS cells and colon carcinoma HT-29 cells through mitochondrial dysfunction and endoplasmic reticulum stress. Apoptosis. 2013 Jul 24. [Epub ahead of print]
[4]. Jiang H， et al. Antidepressant-like effects of curcumin in chronic mild stress of rats: Involvement of its anti-inflammatory action. Prog Neuropsychopharmacol Biol Psychiatry. 2013 Jul 20. pii: S0278-5846(13)00150-4.
[5]. Guo H， et al. Curcumin induces cell cycle arrest and apoptosis of prostate cancer cells by regulating the expression of IkappaBalpha， c-Jun and androgen receptor. Pharmazie. 2013 Jun;68(6):431-4.
[6]. Zhu X， et al. Curcumin alleviates neuropathic pain by inhibiting p300/CBP histone acetyltransferase activity-regulated expression of BDNF and cox-2 in a rat model. PLoS One. 2014 Mar 6;9(3):e91303.
[7]. Balasubramanyam K， et al. Curcumin， a novel p300/CREB-binding protein-specific inhibitor of acetyltransferase， represses the acetylation of histone/nonhistone proteins and histone acetyltransferase-dependent chromatin transcription. J Biol Chem. 2004 Dec 3;279(49):51163-71.
[8]. Jun Wan Shin， et al. Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. Biochem Pharmacol. 2020 Mar;173:113820. |
| 规格 |
1ml |
| 单位 |
瓶 |
中文
英语
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