Sulforaphane is an isothiocyanate present naturally in widely consumed vegetables. Sulforaphane increases tumor suppressor protein transcription and inhibits histone deacetylase activity. Sulforaphane activates Nrf2 and inhibits high glucose-induced progression of pancreatic cancer via AMPK dependent signaling. Sulforaphane has shown anti-cancer and anti-inflammatory activities^[1][2][3][4].

Sulforaphane induces a cell cycle arrest in a dose-dependent manner, followed by cell death. This sulforaphane-induced cell cycle arrest was correlated with an increased expression of cyclins A and B1. Sulforaphane induces cell death via an apoptotic process. Sulforaphane inhibits the reinitiation of growth and diminishes cellular viability in quiescent colon carcinoma cells (HT29) and has a lower toxicity on differentiated CaCo2 cells^[1]. Pre-treatment of H9c2 rat myoblasts with sulforaphane decreases the apoptotic cell number and the expression of pro-apoptotic proteins (Bax, caspase-3 and cytochrome c), as well as the doxorubicin-induced increase in mitochondrial membrane potential. Furthermore, sulforaphane increases the mRNA and protein expression of heme oxygenase-1, which consequently reduces the levels of reactive oxygen species (ROS, measured using MitoSOX Red reagent) in the mitochondria which are induced by doxorubicin^[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Sulforaphane can block the formation of ammary tumors in Sprague-Dawley rats treated with single doses of 9,10-dimethyl-1,2-benzanthracene. Administration of sulforaphane reduces the incidence, multiplicity, and weights and delays the development of the mammary tumors evoked by a single dose of DMBA in female Sprague-Dawley rats^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

177.29

C₆H₁₁NOS₂

4478-93-7

萝卜硫素；莱菔硫烷

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

DMSO : ≥ 62.5 mg/mL (352.53 mM)

* “≥” means soluble, but saturation unknown.

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, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)。-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。

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： 30 % SBE-β-CD

  Solubility: 10 mg/mL (56.40 mM); Clear solution; Need ultrasonic
• 2.

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

  Solubility: ≥ 2.5 mg/mL (14.10 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (14.10 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 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-CD in saline)

  Solubility: ≥ 2.5 mg/mL (14.10 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (14.10 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 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
• 4.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.5 mg/mL (14.10 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (14.10 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Gamet-Payrastre L, et al. Sulforaphane, a naturally occurring isothiocyanate, induces cell cycle arrest and apoptosis in HT29 human colon cancer cells. Cancer Res. 2000 Mar 1;60(5):1426-33.

  [2]. Li B, et al. Sulforaphane prevents doxorubicin-induced oxidative stress and cell death in rat H9c2 cells. Int J Mol Med. 2015 Jul;36(1):53-64.

  [3]. Zhang Y, et al. Anticarcinogenic activities of sulforaphane and structurally related synthetic norbornylisothiocyanates. Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3147-50.

  [4]. Chen X, et al. Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of PancreaticCancer via AMPK Dependent Signaling. ell Physiol Biochem. 2018;50(3):1201-1215.

HT29 cells are seeded at low density (5×10⁴ cells/mL) in 35- or 120-mm diameter Primaria dishes in standard medium containing 5% FCS. One day after seeding, medium is changed, and HT29 cells are treated with sulforaphane (0-30 μM). An equivalent amount of the solvent (ethanol) is added to control cells (0.2% final concentration). Drug effect on cellular viability is evaluated using the MTT assay^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Rats: At age 47, 48, 49, 50, and 51 days, each animal receives by gavage either 0.5 mL of Emulphor EL-620 alone or the specified doses (75, 100, or 150 μM daily) of sulforaphane or compound 2, 3, or 4 in 0.5 mL of Emulphor EL-620. On day 50, 3 hr after administration of the vehicle or protector, all rats also receive an intragastric instillation of 8.0 mg of DMBA dissolved in 1.0 mL of sesame oil. This dose of DMBA is selected to produce a substantial tumor incidence, but not one so high as to overwhelm a potential chemoprotective effect. The animals are examined once weekly for the appearance and location of palpable tumors. At age 202 days, i.e., 152 days after carcinogen administration, all animals are euthanized with ether and weighed. The tumors are separated from fat and connective tissue by dissection, weighed, and fixed in buffered 10% formalin. All tumors are identified microscopically by examination of stained sections^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Gamet-Payrastre L, et al. Sulforaphane, a naturally occurring isothiocyanate, induces cell cycle arrest and apoptosis in HT29 human colon cancer cells. Cancer Res. 2000 Mar 1;60(5):1426-33.

  [2]. Li B, et al. Sulforaphane prevents doxorubicin-induced oxidative stress and cell death in rat H9c2 cells. Int J Mol Med. 2015 Jul;36(1):53-64.

  [3]. Zhang Y, et al. Anticarcinogenic activities of sulforaphane and structurally related synthetic norbornylisothiocyanates. Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3147-50.

  [4]. Chen X, et al. Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of PancreaticCancer via AMPK Dependent Signaling. ell Physiol Biochem. 2018;50(3):1201-1215.