Diallyl Disulfide
(Synonyms: 二烯丙基二硫) 目录号 : GC43437
A natural H2S donor
Cas No.:2179-57-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Diallyl disulfide (DADS) is an organosulfur compound derived from allicin, a natural compound found in garlic and related plants. DADS has diverse physiological effects, many that are cardio- and neuro-protective. These effects are due, at least in part because DADS is converted, in the presence of thiols, to the gaseous mediator hydrogen sulfide (H2S). Thus, DADS serves as a thiol-dependent H2S donor in biological systems.
| Cas No. | 2179-57-9 | SDF | |
| 别名 | 二烯丙基二硫 | ||
| Canonical SMILES | C=CCSSCC=C | ||
| 分子式 | C6H10S2 | 分子量 | 146.3 |
| 溶解度 | DMF: 10 mg/ml,DMF:PBS (pH 7.2) (1:4): 0.2 mg/ml,DMSO: 5 mg/ml,Ethanol: 3 mg/ml | 储存条件 | Store at -20°C |
| 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。 |
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| 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。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 6.8353 mL | 34.1763 mL | 68.3527 mL |
| 5 mM | 1.3671 mL | 6.8353 mL | 13.6705 mL |
| 10 mM | 0.6835 mL | 3.4176 mL | 6.8353 mL |
| 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 | 只 |
| 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 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Diallyl Disulfide and diallyl trisulfide in garlic as novel therapeutic agents to overcome drug resistance in breast cancer
J Pharm Anal 2022 Apr;12(2):221-231.PMID:35582397DOI:10.1016/j.jpha.2021.11.004.
Breast cancer is one of the leading causes of cancer-related deaths in women worldwide. It is a cancer that originates from the mammary ducts and involves mutations in multiple genes. Recently, the treatment of breast cancer has become increasingly challenging owing to the increase in tumor heterogeneity and aggressiveness, which gives rise to therapeutic resistance. Epidemiological, population-based, and hospital-based case-control studies have demonstrated an association between high intake of certain Allium vegetables and a reduced risk in the development of breast cancer. Diallyl Disulfide (DADS) and diallyl trisulfide (DATS) are the main allyl sulfur compounds present in garlic, and are known to exhibit anticancer activity as they interfere with breast cancer cell proliferation, tumor metastasis, and angiogenesis. The present review highlights multidrug resistance mechanisms and their signaling pathways in breast cancer. This review discusses the potential anticancer activities of DADS and DATS, with emphasis on drug resistance in triple-negative breast cancer (TNBC). Understanding the anticancer activities of DADS and DATS provides insights into their potential in targeting drug resistance mechanisms of TNBC, especially in clinical studies.
Diallyl Disulfide prevents 1,3-dichloro-2-propanol-induced hepatotoxicity through mitogen-activated protein kinases signaling
Food Chem Toxicol 2022 Feb;160:112814.PMID:34999178DOI:10.1016/j.fct.2022.112814.
We investigated whether Diallyl Disulfide (DADS) has protective effects against 1,3-dichloro-2-propanol (1,3-DCP)-induced hepatotoxicity and oxidative damage in rats and HepG2 cells. DADS was administered to rats once daily for 7 days at doses of 30 and 60 mg/kg/day. One hour after the final DADS treatment, the rats were administered 90 mg/kg 1,3-DCP to induce acute hepatotoxicity. DADS treatment significantly suppressed the increase in serum aminotransferase levels induced by 1,3-DCP administration, and reduced histopathological alterations in the liver. DADS treatment reduced 1-3-DCP-induced apoptotic changes in the liver, as revealed by terminal deoxynucleotidyl transferase dUTP nick end labeling staining and immunohistochemistry for caspase-3. DADS treatment competitively inhibited or reduced cytochrome p450 2E1 (CYP2E1) expression, which is involved in the metabolic activation of 1,3-DCP, and enhanced antioxidant properties. Furthermore, DADS treatment inhibited phosphorylation of mitogen-activated protein kinases (MAPKs) and apoptotic signaling. In in vitro experiments, MAPKs inhibitors reduced the expression of Bax/Bcl-2/Caspase 3 signaling, which effects were more significant in co-treated cells with DADS and MAPKs inhibitors. In conclusion, the protective effect of DADS against 1,3-DCP-induced hepatotoxicity may be related to blocking the metabolic activation of 1,3-DCP by suppressing CYP2E1 expression, inducing antioxidant enzyme activity, and reducing apoptotic activity by inhibiting phosphorylation of MAPKs.
Diallyl Disulfide prevents cigarette smoke-induced emphysema in mice
Pulm Pharmacol Ther 2021 Aug;69:102053.PMID:34214692DOI:10.1016/j.pupt.2021.102053.
Introduction: Cigarette smoke (CS) is the main risk factor for the development of chronic obstructive pulmonary disease (COPD) and pulmonary emphysema. The use of antioxidants has emerged as a potential therapeutic strategy to treat airway inflammation and lung diseases. In the current study, we investigated the potential therapeutic impact of Diallyl Disulfide (Dads) treatment in a murine model of CS-induced emphysema. Methods: C57BL/6 mice were exposed to CS for 60 consecutive days and treated with vehicle or Dads (30, 60 or 90 mg/kg) by oral gavage for the last 30 days, three times/week. The control group was sham-smoked and received vehicle treatment. All mice were euthanized 24 h after day 60; bronchoalveolar lavage (BAL) was performed and lungs were processed for further experimentation. Histological (HE stained sections, assessment of mean linear intercept (Lm)), biochemical (nitrite, superoxide dismutase (SOD), glutathione transferase (GST), and malondialdehyde (MDA) equivalents), and molecular biology (metalloproteinase (MMP) 12, SOD2, carbonyl reductase 1 (CBR1), nitrotyrosine (PNK), 4-hydroxynonenal (4-HNE), and CYP2E1) analyses were performed. Results: Treatment with Dads dose-dependently reduced CS-induced leukocyte infiltration into the airways (based on BAL fluid counts) and improved lung histology (indicated by a reduction of Lm). Furthermore, CS exposure dramatically reduced the activity of the antioxidant enzymes SOD and GST in lung tissue and increased nitrite and MDA levels in BAL; these effects were all effectively counteracted by Dads treatment. Western blot analysis further confirmed the antioxidant potential of Dads, showing that treatment prevented the CS-induced decrease in SOD2 expression and increase in lung damage markers, such as CBR1, PNK, and 4-HNE. Furthermore, increased MMP12 (an important hallmark of CS-induced emphysema) and CYP2E1 lung protein levels were significantly reduced in mice receiving Dads treatment. Conclusion: Our findings demonstrate that treatment with Dads is effective in preventing multiple pathological features of CS-induced emphysema in an in vivo mouse model. In addition, we have identified several proteins/enzymes, including 4-HNE, CBR1, and CYP2E1, that are modifiable by Dads and could represent specific therapeutic targets for the treatment of COPD and emphysema.
A comprehensive understanding about the pharmacological effect of Diallyl Disulfide other than its anti-carcinogenic activities
Eur J Pharmacol 2021 Feb 15;893:173803.PMID:33359648DOI:10.1016/j.ejphar.2020.173803.
Diallyl Disulfide (DADS), an oil-soluble sulfur compound that is responsible for the biological effects of garlic, displays numerous biological activities, among which its anti-cancer activities are the most famous ones. In recent years, the pharmacological effects of DADS other than its anti-carcinogenic activities have attracted numerous attentions. For example, it has been reported that DADS can prevent the microglia-mediated neuroinflammatory response and depression-like behaviors in mice. In the cardiovascular system, DADS administration was found to ameliorate the isoproterenol- or streptozotocin-induced cardiac dysfunction via the activation of the nuclear factor E2-related factor 2 (Nrf2) and insulin-like growth factor (IGF)-phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) signaling. DADS administration can also produce neuroprotective effects in animal models of Alzheimer's disease and protect the heart, endothelium, liver, lung, and kidney against cellular or tissue damages induced by various toxic factors, such as the oxidized-low density lipoprotein (ox-LDL), carbon tetrachloride (CCl4), ethanol, acetaminophen, Cis-Diammine Dichloroplatinum (CisPt), and gentamicin. The major mechanisms of action of DADS in disease prevention and/or treatment include inhibition of inflammation, oxidative stress, and cellular apoptosis. Mechanisms, including the activation of Akt, extracellular signal-regulated kinase 1/2 (ERK1/2), protein kinase A (PKA), and cyclic adenosine monophosphate-response element binding protein (CREB) and the inhibition of histone deacetylases (HDACs), can also mediate the cellular protective effects of DADS in different tissues and organs. In this review, we summarize and discuss the pharmacological effects of DADS other than its anti-carcinogenic activities, aiming to reveal more possibilities for DADS in disease prevention and/or treatment.
Diallyl Disulfide suppresses the lipopolysaccharide-driven inflammatory response of macrophages by activating the Nrf2 pathway
Food Chem Toxicol 2022 Jan;159:112760.PMID:34896185DOI:10.1016/j.fct.2021.112760.
Lipopolysaccharide (LPS)-driven activation of Kupffer cells plays critical roles in the development of alcoholic liver disease (ALD). Accumulating evidence has revealed that nuclear factor erythroid 2-related factor 2 (Nrf2) can modulate the polarization of macrophages. The current study aimed to investigate the roles of Diallyl Disulfide (DADS) in LPS-driven inflammation in vitro and in vivo. We found that DADS significantly increased the nuclear translocation of Nrf2 and the transcription of Nrf2 targets, including HO1, NQO1, and γ-GCSc, and suppressed degradation of Nrf2 protein. Besides, DADS significantly inhibited LPS-induced activation of NF-κB and MAPK, secretion of NO and TNF-α, and production of reactive oxygen species (ROS) in LPS-exposed RAW264.7 cells. In vivo study demonstrated that DADS significantly ameliorated liver damage in mice challenged with LPS, as shown by the inhibition of increases in serum aminotransferase activities, neutrophil infiltration, and NF-κB and NLRP3 inflammasome activation. Finally, knockout of Nrf2 abrogated the suppression of DADS on macrophage polarization and on liver injury induced by LPS. These findings reveal that DADS suppresses LPS-driven inflammatory response in the liver by activating Nrf2, which suggests that the protective effects of DADS against ALD may be attributed to the modulation of Kupffer cell polarization in the liver.