Curcumin (Diferuloylmethane), a natural phenolic compound, is ap300/CREB-binding protein-specificinhibitor of acetyltransferase, represses the acetylation of histone/nonhistone proteins and histone acetyltransferase-dependent chromatin transcription. Curcumin shows inhibitory effects onNF-κBandMAPKs, and has diverse pharmacologic effects including anti-inflammatory, antioxidant, antiproliferative and antiangiogenic activities. Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification.

Keap1-Nrf2^[1], Histone acetyltransferase^[6]

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 IC₅₀is 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].

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].

368.38

Solid

C₂₁H₂₀O₆

458-37-7

姜黄素；酸性黄；姜黄色素

• Phenols
• Polyphenols

• Plants
• Zingiberaceae
• Curcuma longa

Room temperature in continental US; may vary elsewhere.

DMSO : 120 mg/mL(325.75 mM;Need ultrasonic)

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℃, 6 months; -20℃, 1 month。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 1% (w/v) carboxymethylcellulose (CMC)

  Solubility: 25 mg/mL (67.86 mM); Suspension solution; Need ultrasonic
• 2.

  请依序添加每种溶剂： 10% DMSO    40%PEG300   5%Tween-80   45% saline

  Solubility: ≥ 3 mg/mL (8.14 mM); Clear solution

  此方案可获得 ≥ 3 mg/mL (8.14 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 30.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH2O 中，得到澄清透明的生理盐水溶液
• 3.

  请依序添加每种溶剂： 10% DMSO    90% (20%SBE-β-CDin saline)

  Solubility: 3 mg/mL (8.14 mM); Suspended solution; Need ultrasonic

  此方案可获得 3 mg/mL (8.14 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

  以 1 mL 工作液为例，取 100 μL 30.0 mg/mL 的澄清 DMSO 储备液加到 900 μL20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明