Mogrol
(Synonyms: 罗汉果醇) 目录号 : GC32789
Mogrol是罗汉果甜甙的生物代谢物，能够抑制ERK1/2和STAT3的信号通路，同时能降低CREB的活性，活化AMPK。
Cas No.:88930-15-8
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | Cell viability is determined with a MTT assay. Leukemia cells are plated in triplicate into a 96-well plate. After overnight incubation, they are treated with various concentrations of mogrol (0, 0.1, 1, 10, 100, 200 and 250 µM) for 24 h and 48 h. The percentage of viable cells is calculated as the ratio (A490) of treated cells over control cells. Triplicate experiments are performed. |
References: [1]. Liu C, et al. Mogrol represents a novel leukemia therapeutic, via ERK and STAT3 inhibition. Am J Cancer Res. 2015 Mar 15;5(4):1308-18. | |
Mogrol is a biometabolite of mogrosides, and acts via inhibition of the ERK1/2 and STAT3 pathways, or reducing CREB activation and activating AMPK signaling.
Mogrol (0-250 µM) significantly and dose- and time-dependently inhibits K562 cell growth and increases the number of apoptotic cells. Mogrol (0, 10, 100, and 250 µM) induces G1 phase cell cycle arrest in K562 cells. Treatment with mogrol significantly decreases ERK phosphorylation as compared to control cells, whereas total ERK protein is not affected. Mogrol dose-dependently induces growth arrest in G0/G1 phase of the cell cycle. Mogrol significantly and dose-dependently enhances p21 protein expression in K562 cells[1]. Mogrol significantly represses the increase in cellular TG levels induced by differentiation stimuli, and suppresses TG accumulation at micromolar levels, with a statistically significant suppression observed above 10 μM. Mogrol suppresses adipogenesis in 3T3-L1 cells at concentrations that does not affect cell viability. Mogrol suppresses adipogenesis through at least two different mechanisms, increasing AMPK phosphorylation and repressing the activation of CREB[2].
[1]. Liu C, et al. Mogrol represents a novel leukemia therapeutic, via ERK and STAT3 inhibition. Am J Cancer Res. 2015 Mar 15;5(4):1308-18. [2]. Naoki Harada, et al. Mogrol Derived from Siraitia grosvenorii Mogrosides Suppresses 3T3-L1 Adipocyte Differentiation by Reducing cAMP-Response Element-Binding Protein Phosphorylation and Increasing AMP-Activated Protein Kinase Phosphorylation. PLoS One. 2
| Cas No. | 88930-15-8 | SDF | |
| 别名 | 罗汉果醇 | ||
| Canonical SMILES | CC1(C)[C@@H](O)CC[C@@]2([H])[C@]3(C)[C@H](O)C[C@]4(C)[C@@H]([C@H](C)CC[C@@H](O)C(C)(O)C)CC[C@](C)4[C@]3([H])CC=C12 | ||
| 分子式 | C30H52O4 | 分子量 | 476.73 |
| 溶解度 | Soluble in DMSO | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.0976 mL | 10.4881 mL | 20.9762 mL |
| 5 mM | 0.4195 mL | 2.0976 mL | 4.1952 mL |
| 10 mM | 0.2098 mL | 1.0488 mL | 2.0976 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。
Mogrol, an aglycone of mogrosides, attenuates ulcerative colitis by promoting AMPK activation
Phytomedicine 2021 Jan;81:153427.PMID:33296813DOI:10.1016/j.phymed.2020.153427.
Background: Ulcerative colitis (UC) is a non-specific chronic inflammatory disease. The incidence of UC in China has been increasing in recent years. Mogrol is an aglycone of mogrosides. Studies have shown that mogrosides have anti-oxygenation, anti-inflammatory, and laxative effects as well as other biological activities. Purpose: To investigate the beneficial effects of Mogrol on UC and identify its underlying mechanisms. Study design: We used the dextran sodium sulphate (DSS)-induced UC model in mice, TNF-α-damaged NCM460 colonic epithelial cells, macrophage cells THP-M stimulated with lipopolysaccharide (LPS) / adenosine triphosphate (ATP) and compound C (an AMPK inhibitor) to confirm the key role of AMPK (AMP-activated protein kinase) activation. Methods: Histological evaluation, immunohistochemical staining, Western blot analysis, immunofluorescence assay and quantitative real time-PCR were used in the study. Results: Oral administration of Mogrol (5 mg/kg/daily) in vivo significantly attenuated pathological colonic damage, inhibited inflammatory infiltration and improved the abnormal expression of NLRP3 inflammasome in colonic mucosa via the AMPK and NF-κB signaling pathways. In vitro, Mogrol protected against intestinal epithelial barrier dysfunction by activating AMPK in TNF-α-treated NCM460 cells and inhibited the production of inflammatory mediator in LPS-stimulated THP-M cells. Furthermore, Mogrol's effects were reversed by compound C intervention in DSS-induced UC model. Conclusion: Mogrol exerts protective effects in experimental UC and inhibits production of inflammatory mediators through activation of AMPK-mediated signaling pathways.
Pharmacological Activities of Mogrol: Potential Phytochemical against Different Diseases
Life (Basel) 2023 Feb 16;13(2):555.PMID:36836915DOI:10.3390/life13020555.
Recently, Mogrol has emerged as an important therapeutic candidate with multiple potential pharmacological properties, including neuroprotective, anticancer, anti-inflammatory, antiobesity, antidiabetes, and exerting a protective effect on different organs such as the lungs, bone, brain, and colon. Pharmacokinetic studies also highlighted the potential of Mogrol as a therapeutic. Studies were also conducted to design and synthesize the analogs of Mogrol to achieve better activities against different diseases. The literature also highlighted the possible molecular mechanism behind pharmacological activities, which suggested the role of several important targets, including AMPK, TNF-α, and NF-κB. These important Mogrol targets were verified in different studies, indicating the possible role of Mogrol in other associated diseases. Still, the compilation of pharmacological properties, possible molecular mechanisms, and important targets of the Mogrol is missing in the literature. The current study not only provides the compilation of information regarding pharmacological activities but also highlights the current gaps and suggests the precise direction for the development of Mogrol as a therapeutic against different diseases.
Design and synthesis of Mogrol derivatives modified on a ring with anti-inflammatory and anti-proliferative activities
Bioorg Med Chem Lett 2022 Oct 15;74:128924.PMID:35944853DOI:10.1016/j.bmcl.2022.128924.
A class of novel Mogrol derivatives modified on A ring were synthesized. The screening result showed that indole-fused derivatives exhibited lower toxicity and better anti-inflammatory activity in LPS-induced RAW 264.7 cells model than Mogrol and other compounds. Derivative B8 exerted superior inhibitory result of NO production (IC50 = 5.05 μM) and inhibitory ability of TNF-α and IL-6 secretion to Mogrol through iNOS/NF-κB pathway. Besides, the CCK8 assay was performed to evaluate their anti-proliferative activity against non-small cell lung cancer including A549, NCI-H460, H1299 and H1975 cells. Compared with Mogrol, compound B8 showed moderate anti-proliferative activities against A549 and H1975 cells, while derivatives bearing α, β-unsaturated ketone scaffold displayed broad-spectrum growth inhibition against four cell lines. Among them, compound A9 showed 12-fold higher activity than Mogrol against H1299 and H1975 cells. The suppressive effect on expression level of p-p65 might account for the compound A9-induced growth inhibition and cell cycle arrest at G1 phase.
Mogrol suppresses lung cancer cell growth by activating AMPK-dependent autophagic death and inducing p53-dependent cell cycle arrest and apoptosis
Toxicol Appl Pharmacol 2022 Jun 1;444:116037.PMID:35489526DOI:10.1016/j.taap.2022.116037.
Lung carcinoma is the leading cause of cancer-related death worldwide. Chemotherapy remains the cornerstone of lung cancer treatment. Unfortunately, most types of cancer will develop resistance to chemotherapies over the time. One of the efforts to prevent the chemotherapy resistance is to find alternative chemotherapy drugs. Mogrol has been found to have antitumor activity. However, little is known about the pharmacological mechanisms underlying the suppression of Mogrol on lung cancers. In this study, we observed that Mogrol exposure significantly reduced the tumor volume and weight in tumor-bearing nude mice without obvious effect on body weight and cardiac function. Mogrol also significantly inhibited the proliferation and migration of lung cancer cells, including non-small-cell lung carcinoma cells, A549, H1299, H1975 and SK-MES-1 cells, with no obvious effect on control human bronchial epithelial cells (HBE). Further studies revealed that Mogrol stirred excessive autophagy and autophagic flux, and finally, autophagic cell death, in lung cancer cells, which could be attenuated by autophagy inhibitors, 3-MA and chloroquine. Furthermore, Mogrol significantly activated AMPK to induce autophagy and autophagic cell death, which could be abrogated by Compound C, an AMPK inhibitor. In addition, Mogrol induced a significant increase in p53 activity in lung cancer cells, accompanied with cell cycle arrest and apoptosis, which could be weakened by p53 silence. Our results indicated that Mogrol effectively suppressed lung cancer cells in vivo and in vitro by inducing the excessive autophagy and autophagic cell death via activating AMPK signaling pathway, as well as cell cycle arrest and apoptosis via activating p53 pathway.
Mogrol Attenuates Osteoclast Formation and Bone Resorption by Inhibiting the TRAF6/MAPK/NF-κB Signaling Pathway In vitro and Protects Against Osteoporosis in Postmenopausal Mice
Front Pharmacol 2022 Mar 9;13:803880.PMID:35496311DOI:10.3389/fphar.2022.803880.
Osteoporosis is a serious public health problem that results in fragility fractures, especially in postmenopausal women. Because the current therapeutic strategy for osteoporosis has various side effects, a safer and more effective treatment is worth exploring. It is important to examine natural plant extracts during new drug design due to low toxicity. Mogrol is an aglycon of mogroside, which is the active component of Siraitia grosvenorii (Swingle) and exhibits anti-inflammatory, anticancer and neuroprotective effects. Here, we demonstrated that Mogrol dose-dependently inhibited osteoclast formation and function. To confirm the mechanism, RNA sequencing (RNA-seq), real-time PCR (RT-PCR), immunofluorescence and Western blotting were performed. The RNA-seq data revealed that Mogrol had an effect on genes involved in osteoclastogenesis. Furthermore, RT-PCR indicated that Mogrol suppressed osteoclastogenesis-related gene expression, including CTSK, ACP5, MMP9 and DC-STAMP, in RANKL-induced bone marrow macrophages Western blotting demonstrated that Mogrol suppressed osteoclast formation by blocking TNF receptor-associated factor 6 (TRAF6)-dependent activation of the mitogen-activated protein kinase nuclear factor-B (NF-κB) signaling pathway, which decreased two vital downstream transcription factors, the nuclear factor of activated T cells calcineurin-dependent 1 (NFATc1) and c-Fos proteins expression. Furthermore, Mogrol dramatically reduced bone mass loss in postmenopausal mice. In conclusion, these data showed that Mogrol may be a promising procedure for osteoporosis prevention or therapy.