Fargesin
(Synonyms: 辛夷脂素) 目录号 : GC38183
Fargesin is a neolignan isolated from Magnolia plants. It is a potential β1AR antagonist through cAMP/PKA pathway.
Cas No.:31008-19-2
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
Fargesin is a neolignan isolated from Magnolia plants. It is a potential β1AR antagonist through cAMP/PKA pathway.
| Cas No. | 31008-19-2 | SDF | |
| 别名 | 辛夷脂素 | ||
| Canonical SMILES | COC1=CC=C([C@H]2OC[C@@]3([H])[C@H](C4=CC=C(OCO5)C5=C4)OC[C@]32[H])C=C1OC | ||
| 分子式 | C21H22O6 | 分子量 | 370.4 |
| 溶解度 | DMSO: 125 mg/mL (337.47 mM) | 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 | 2.6998 mL | 13.4989 mL | 26.9978 mL |
| 5 mM | 0.54 mL | 2.6998 mL | 5.3996 mL |
| 10 mM | 0.27 mL | 1.3499 mL | 2.6998 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。
Fargesin ameliorates osteoarthritis via macrophage reprogramming by downregulating MAPK and NF-κB pathways
Arthritis Res Ther 2021 May 14;23(1):142.PMID:33990219DOI:10.1186/s13075-021-02512-z.
Background: To investigate the role and regulatory mechanisms of Fargesin, one of the main components of Magnolia fargesii, in macrophage reprogramming and crosstalk across cartilage and synovium during osteoarthritis (OA) development. Methods: Ten-week-old male C57BL/6 mice were randomized and assigned to vehicle, collagenase-induced OA (CIOA), or CIOA with intra-articular Fargesin treatment groups. Articular cartilage degeneration was evaluated using the Osteoarthritis Research Society International (OARSI) score. Immunostaining and western blot analyses were conducted to detect relative protein. Raw264.7 cells were treated with LPS or IL-4 to investigate the role of polarized macrophages. ADTC5 cells were treated with IL-1β and conditioned medium was collected to investigate the crosstalk between chondrocytes and macrophages. Results: Fargesin attenuated articular cartilage degeneration and synovitis, resulting in substantially lower Osteoarthritis Research Society International (OARSI) and synovitis scores. In particular, significantly increased M2 polarization and decreased M1 polarization in synovial macrophages were found in fargesin-treated CIOA mice compared to controls. This was accompanied by downregulation of IL-6 and IL-1β and upregulation of IL-10 in serum. Conditioned medium (CM) from M1 macrophages treated with Fargesin reduced the expression of matrix metalloproteinase-13, RUNX2, and type X collagen and increased Col2a1 and SOX9 in OA chondrocytes, but Fargesin alone did not affect chondrocyte catabolic processes. Moreover, Fargesin exerted protective effects by suppressing p38/ERK MAPK and p65/NF-κB signaling. Conclusions: This study showed that Fargesin switched the polarized phenotypes of macrophages from M1 to M2 subtypes and prevented cartilage degeneration partially by downregulating p38/ERK MAPK and p65/NF-κB signaling. Targeting macrophage reprogramming or blocking the crosstalk between macrophages and chondrocytes in early OA may be an effective preventive strategy.
Protective effects of Fargesin on cadmium-induced lung injury through regulating aryl hydrocarbon receptor
J Biochem Mol Toxicol 2022 Nov;36(11):e23197.PMID:35983679DOI:10.1002/jbt.23197.
Fragesin, a traditional Chinese medicine, has been shown to exert anti-inflammatory effect. The aim of this study was to figure out the possible effectiveness of the Fargesin, and to invest the mechanisms by which it works in the cadmium-induced lung injury in mice. Fargesin was given 1 h before cadmium treatment for 7 days. Then, the bronchoalveolar lavage fluid (BALF) were harvested to test inflammatory cells and pro-inflammatory cytokine production. Lung histopathological changes, myeloperoxidase (MPO) activity, and aryl hydrocarbon receptor (AhR) and nuclear factor kappa B (NF-κB) activation were measured. Fargesin dose-dependently reduced inflammatory cells and pro-inflammatory cytokines in BALF, improved lung histopathological injury, and inhibited lung wet/dry ratio and MPO activity. Furthermore, Fargesin inhibited cadmium-induced NF-κB activation. In addition, Fargesin was found to increase AhR expression. In conclusion, Fargesin attenuates cadmium-induced lung injury may be via activating AhR, which subsequently suppressing the inflammatory response.
Fargesin alleviates atherosclerosis by promoting reverse cholesterol transport and reducing inflammatory response
Biochim Biophys Acta Mol Cell Biol Lipids 2020 May;1865(5):158633.PMID:31988050DOI:10.1016/j.bbalip.2020.158633.
Background and aims: Fargesin mainly functions in the improvement of lipid metabolism and the inhibition of inflammation, but the role of Fargesin in atherogenesis and the molecular mechanisms have not been defined. We aimed to explore if and how Fargesin affects atherosclerosis by regulating lipid metabolism and inflammatory response. Methods and results: ApoE-/- mice were fed a high-fat diet to form atherosclerotic plaques and then administrated with Fargesin or saline via gavage. Oil Red O, HE and Masson staining were performed to assess atherosclerostic plaques in apoE-/- mice. [3H] labeled cholesterol was used to detect cholesterol efflux and reverse cholesterol transport (RCT) efficiency. Enzymatic methods were performed to analyze plasma lipid profile in apoE-/- mice. Immunohistochemistry was used to analyze macrophage infiltration. THP-1-derived macrophages were incubated with Fargesin or not. Both Western blot and qRT-PCR were applied to detect target gene expression. Oil Red O staining was applied to examine lipid accumulation in THP-1-derived macrophages. ELISA and qRT-PCR were used to examine the levels of inflammatory mediotors. We found that Fargesin reduced atherosclerotic lesions by elevating efficiency of RCT and decreasing inflammatory response via upregulation of ABCA1 and ABCG1 expression in apoE-/- mice. Further, Fargesin reduced lipid accumulation in THP-1-derived macrophages. Besides, Fargesin increased phosphorylation of CEBPα in Ser21 and then upregulated LXRα, ABCA1 and ABCG1 expression in THP-1-derived macrophages. In addition, Fargesin could reduce ox-LDL-induced inflammatory response by inactivation of the TLR4/NF-κB pathway. Conclusion: These results suggest that Fargesin inhibits atherosclerosis by promoting RCT process and reducing inflammatory response via CEBPαS21/LXRα and TLR4/NF-κB pathways, respectively.
Fargesin Inhibits EGF-Induced Cell Transformation and Colon Cancer Cell Growth by Suppression of CDK2/Cyclin E Signaling Pathway
Int J Mol Sci 2021 Feb 19;22(4):2073.PMID:33669811DOI:10.3390/ijms22042073.
Although the lignan compound Fargesin is a major ingredient in Shin-Yi, the roles of Fargesin in carcinogenesis and cancer cell growth have not been elucidated. In this study, we observed that Fargesin inhibited cell proliferation and transformation by suppression of epidermal growth factor (EGF)-stimulated G1/S-phase cell cycle transition in premalignant JB6 Cl41 and HaCaT cells. Unexpectedly, we found that signaling pathway analyses showed different regulation patterns in which Fargesin inhibited phosphatidylinositol 3-kinase/AKT signaling without an alteration of or increase in mitogen activated protein kinase (MAPK) in JB6 Cl41 and HaCaT cells, while both signaling pathways were abrogated by Fargesin treatment in colon cancer cells. We further found that fargesin-induced colony growth inhibition of colon cancer cells was mediated by suppression of the cyclin dependent kinase 2 (CDK2)/cyclin E signaling axis by upregulation of p21WAF1/Cip1, resulting in G1-phase cell cycle accumulation in a dose-dependent manner. Simultaneously, the suppression of CDK2/cyclin E and induction of p21WAF1/Cip1 were correlated with Rb phosphorylation and c-Myc suppression. Taken together, we conclude that fargesin-mediated c-Myc suppression inhibits EGF-induced cell transformation and colon cancer cell colony growth by the suppression of retinoblastoma (Rb)-E2F and CDK/cyclin signaling pathways, which are mainly regulated by MAPK and PKB signaling pathways.
Fargesin inhibits melanin synthesis in murine malignant and immortalized melanocytes by regulating PKA/CREB and P38/MAPK signaling pathways
J Dermatol Sci 2019 Apr;94(1):213-219.PMID:30956031DOI:10.1016/j.jdermsci.2019.03.004.
Background: Fargesin is commonly used in the treatment of allergic rhinitis, inflammation, sinusitis and headache. Objective: The aim of the study is to investigate a new function of Fargesin against melanin production and its underlying molecular mechanism. Methods: B16F10 mouse melanoma cells, Melan-a and human epidermal melanocytes were treated with different concentrations of Fargesin for the indicated time. The extracellular and cellular melanin content was detected by spectrometry at 490 nm and 405 nm, respectively. RT-qPCR and Western blot analysis were used to exam the expression of melanogenic enzymes and the activities of PKA/CREB and p38 MAPK pathway components. Zebrafish was used as an in vivo model for studying the function of Fargesin in regulating melanogenesis. Results: Fargesin effectively inhibited melanin production at moderate dose in mouse B16F10 melanoma cells, normal melanocyte cell lines and zebrafish. The expression of microphthalmia-associated transcription factor (MITF), its downstream melanogenic enzymes and tyrosinase activity were also strongly reduced by Fargesin. Moreover, the increase of melanin production induced by UVB and forskolin could be fully reversed by Fargesin treatment. Fargesin also effectively inhibited the activation of PKA/CREB and p38 MAPK as well as their interactions, which in turn is responsible for the expression of MITF and melanogenic enzymes. Conclusions: These results show that Fargesin can function as an anti-melanogenic agent, at least in part, by inhibiting PKA/CREB and p38/MAPK signaling pathways. Therefore, Fargesin and its derivatives may potentially be used for preventing hyperpigmentation disorders in the future.