S-Allylmercaptocysteine
目录号 : GC63933
S-allylmercaptocysteine 是一种从大蒜中提取的有机硫化合物，对各种肺部疾病具有抗炎和抗氧化作用。S-allylmercaptocysteine 通过多种途径发挥抗癌作用，如通过 TGF-β 信号通路诱导癌细胞凋亡 (apoptosis)，或通过降低 NF-κb 活性和上调 Nrf2 来达到抗炎和抗氧化的作用。
Cas No.:2281-22-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
S-allylmercaptocysteine, an organic sulfur compound extracted from garlic, has anti-inflammatory and anti-oxidative effects for various pulmonary diseases. S-allylmercaptocysteine achieves its anti-cancer effect through a variety of pathways such as inducing the apoptosis of cancer cells through the TGF-β signaling pathway, or reducing the NF-κB activity and up-regulating Nrf2 to achieve the effects of anti-inflammation and anti-oxidation[1][2][3].
S-Allylmercaptocysteine attenuates cisplatin-induced nephrotoxicity through suppression of apoptosis, oxidative stress, and inflammation[2].S-Allylmercaptocysteine (400 μM; 48 hours) induces apoptosis evaluated by detecting the activated caspase 3 and cleaved PARP in SW620, SW480, and Caco-2 cells. Both activated caspase 3 and cleaved PARP1 are found in the cells treated with SAMC while no activated PARP1 and caspase 3 are found in the untreated control cells[4].
S-Allylmercaptocysteine (25 and 50 mg/kg; oral gavage) could significantly ameliorate the pathological structure, and decrease inflammatory cell infiltration and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) in BLM-induced pulmonary fibrosis mice. S-Allylmercaptocysteine shows an anti-fibrosis effect by increasing anti-oxidants like HO-1, GSH and SOD as well as decreasing hydroxyproline (HYP) in BLM-induced mice[1].
[1]. Tong D, et al. S-allylmercaptocysteine promotes MAPK inhibitor-induced apoptosis by activating the TGF-β signaling pathway in cancer cells. Oncol Rep. 2014;32(3):1124-1132.
[2]. Zhu X, et al. S-Allylmercaptocysteine Attenuates Cisplatin-Induced Nephrotoxicity through Suppression of Apoptosis, Oxidative Stress, and Inflammation. Nutrients. 2017;9(2):166. Published 2017 Feb 20.
[3]. Li C, et al. S-Allylmercaptocysteine attenuates Bleomycin-induced pulmonary fibrosis in mice via suppressing TGF-β1/Smad and oxidative stress pathways. Int Immunopharmacol. 2020;79:106110.
[4]. Liang D, et al. S-allylmercaptocysteine effectively inhibits the proliferation of colorectal cancer cells under in vitro and in vivo conditions. Cancer Lett. 2011;310(1):69-76.
| Cas No. | 2281-22-3 | SDF | Download SDF |
| 分子式 | C6H11NO2S2 | 分子量 | 193.29 |
| 溶解度 | H2O : 1 mg/mL (5.17 mM; ultrasonic and warming and heat to 60°C); DMSO : < 1 mg/mL (insoluble or slightly soluble) | 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 | 5.1736 mL | 25.8679 mL | 51.7357 mL |
| 5 mM | 1.0347 mL | 5.1736 mL | 10.3471 mL |
| 10 mM | 0.5174 mL | 2.5868 mL | 5.1736 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。
S-Allylmercaptocysteine improves alcoholic liver disease partly through a direct modulation of insulin receptor signaling
Acta Pharm Sin B 2021 Mar;11(3):668-679.PMID:33777674DOI:10.1016/j.apsb.2020.11.006.
Alcoholic liver disease (ALD) causes insulin resistance, lipid metabolism dysfunction, and inflammation. We investigated the protective effects and direct regulating target of S-Allylmercaptocysteine (SAMC) from aged garlic on liver cell injury. A chronic ethanol-fed ALD in vivo model (the NIAAA model) was used to test the protective functions of SAMC. It was observed that SAMC (300 mg/kg, by gavage method) effectively ameliorated ALD-induced body weight reduction, steatosis, insulin resistance, and inflammation without affecting the health status of the control mice, as demonstrated by histological, biochemical, and molecular biology assays. By using biophysical assays and molecular docking, we demonstrated that SAMC directly targeted insulin receptor (INSR) protein on the cell membrane and then restored downstream IRS-1/AKT/GSK3β signaling. Liver-specific knock-down in mice and siRNA-mediated knock-down in AML-12 cells of Insr significantly impaired SAMC (250 μmol/L in cells)-mediated protection. Restoration of the IRS-1/AKT signaling partly recovered hepatic injury and further contributed to SAMC's beneficial effects. Continuous administration of AKT agonist and recombinant IGF-1 in combination with SAMC showed hepato-protection in the mice model. Long-term (90-day) administration of SAMC had no obvious adverse effect on healthy mice. We conclude that SAMC is an effective and safe hepato-protective complimentary agent against ALD partly through the direct binding of INSR and partial regulation of the IRS-1/AKT/GSK3β pathway.
Anti-cancer activities of S-Allylmercaptocysteine from aged garlic
Chin J Nat Med 2019 Jan;17(1):43-49.PMID:30704623DOI:10.1016/S1875-5364(19)30008-1.
While most types of malignancies remain recalcitrant to treatment, application of natural products or their analogs in daily life has offered some hopes as an effective prophylaxis against cancer onset and progression in the past decades. Emerging evidence supports a link between garlic consumption and decreased cancer incidence. Notably, aged garlic extract (AGE) exhibits stronger anti-cancer activities than that of fresh garlic, by virtue of enrichment of several AGE-specific organosulfur compounds, including S-Allylmercaptocysteine (SAMC). In this review, we summarize the up-to-date mechanistic pathways associated with the anti-proliferative, anti-metastatic and pro-apoptotic effects of SAMC in various cancer models. Based upon the proven safety and improved understanding on its anti-neoplastic properties, SAMC has gained recognition as a promising daily food supplement for cancer prevention or management.
S-Allylmercaptocysteine promotes anti-tumor immunity by suppressing PD-L1 expression
Biomed Pharmacother 2023 May;161:114446.PMID:37002570DOI:10.1016/j.biopha.2023.114446.
SAMC (S-Allylmercaptocysteine) possesses significant anti-tumor effects and is proven to inhibit inflammation in chronic obstructive pulmonary disease. The potential to regulate the immune system of SAMC inspired us to detect whether SAMC can promote anti-tumor immunity. Here we found that SAMC inhibits tumor development and progression by boosting CD8+ T cell and NK cell infiltration and decreasing the frequency of immune suppressing Treg cells in tumor tissue and enhancing the systemic immune function. Mechanistically, we found that SAMC suppresses PD-L1 expression at transcriptional level to increase the activation of anti-tumor cytotoxic T cells. Finally, we proved that SAMC inhibits PD-L1 transcription by suppressing the phosphorylation activation of STAT3. In conclusion, our findings reveal that SAMC is a potent immunity regulator and a potential agent for immune checkpoint inhibition in tumor therapy.
S-Allylmercaptocysteine Targets Nrf2 in Osteoarthritis Treatment Through NOX4/NF-κB Pathway
Drug Des Devel Ther 2020 Oct 28;14:4533-4546.PMID:33149551DOI:10.2147/DDDT.S258973.
Purpose: This study aimed to explore the potential role and mechanism of garlic-derived S-Allylmercaptocysteine (SAMC), the major water-soluble fraction of garlic, in osteoarthritis (OA) both in vivo and in vitro. Methods: The effect of SAMC in a surgical-induced OA model was examined by X-ray, staining, ELISA, and immunoblotting. Then the key role of Nrf2 by SAMC treatment in IL-1β stimulated chondrocytes in vitro was determined by gene-knockdown technique. Results: SAMC could stabilize the extracellular matrix (ECM) by decreasing metalloproteinase (MMPs) expression to suppress type II collagen degradation in OA rats. The inflammatory cytokines, such as IL-1β, TNF-α, and IL-6, were elevated in OA, which could be down-regulated by SAMC treatment. This effect was parallel with NF-κB signaling inhibition by SAMC. As oxidative stress has been shown to participate in the inflammatory pathways in OA conditions, the key regulator Nrf2 in redox-homeostasis was evaluated in SAMC-treated OA rats. Nrf2 and its down-stream gene NQO-1 were activated in the SAMC-treated group, accompanied by NAD(P)H oxidases 4 (NOX4) expression down-regulated. As a result, the toxic lipid peroxidation byproduct 4-hydroxynonenal (4HNE) was reduced in articular cartilage. In IL-1β-stimulated primary rat chondrocytes, which could mimic OA in vitro, SAMC could ameliorate collagen destruction, inhibit inflammation, and maintain redox-homeostasis. Interestingly, after Nrf2 gene knockdown by adenovirus, the protective effect of SAMC in IL-1β-stimulated chondrocytes disappeared. Conclusion: Overall, our study demonstrated that SAMC targeted Nrf2 to protect OA both in vivo and in vitro, which would be a new pharmaceutical way for OA therapy.
S-Allylmercaptocysteine improves nonalcoholic steatohepatitis by enhancing AHR/NRF2-mediated drug metabolising enzymes and reducing NF-κB/IκBα and NLRP3/6-mediated inflammation
Eur J Nutr 2021 Mar;60(2):961-973.PMID:32556446DOI:10.1007/s00394-020-02305-1.
Purpose: To investigate the novel molecular mechanisms of the antioxidant and anti-inflammatory properties of S-Allylmercaptocysteine (SAMC) based on a transcriptomic study in a nonalcoholic steatohepatitis (NASH) rat model METHODS: NASH was induced in Sprague-Dawley rats by feeding with a high fat diet (HFD) for 12 weeks. 200 mg/kg SAMC was fed by oral gavage for 4 weeks from 9 to 12 week. Results: SAMC co-administration attenuated HFD-induced liver injury, including the increased serum ALT, hepatic oxidative stress and inflammation. Transcriptomic analysis revealed that SAMC dramatically induced the XRE- and ARE-driven drug metabolising enzymes (DMEs) including Akr7a3, Akr1b8, and Nqo1. The nuclear translocation of the upstream regulator of xenobiotics metabolism, AHR, and regulator of antioxidant responses, NRF2, were significantly increased by SAMC treatment. Furthermore, SAMC counteracted the effects of HFD on NF-κB/IκB and NLRP3/6 pathways with decreasing protein levels of ASC, cleaved caspase-1, IL-18, and IL-1β. These results were further verified in another mice NASH model induced by an MCD diet with SAMC co-administration. Conclusion: We propose that SAMC triggers AHR/NRF2-mediated antioxidant responses which may further suppress the NLRP3/6 inflammasome pathway and NF-κB activation, contributing to the improvement of NASH.