Vulpinic Acid
(Synonyms: 吴耳酸) 目录号 : GC45595
A lichen metabolite with diverse biological activities
Cas No.:521-52-8
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
Vulpinic acid is a lichen metabolite that has been found in L. vulpina and has diverse biological activities.1,2,3,4 It is active against C. perfringens, B. vulgatus, B. fragilis, B. loescheii, P. acnes, E. faecium, and methicillin-susceptible and -resistant S. aureus (MICs = 4-16 μg/ml).1 Vulpinic acid (25-800 μM) prevents UVB-induced apoptosis, cytotoxicity, and cytoskeletal modifications in HaCaT human keratinocytes.2 It also increases scratch wound healing of HaCaT cells.3 Vulpinic acid (15 μM) reduces hydrogen peroxide-induced production of reactive oxygen species (ROS) and cytotoxicity in human umbilical vein endothelial cells (HUVECs).4
References
1. Lauterwein, M., Oethinger, M., Belsner, K., et al. In vitro activities of the lichen secondary metabolites vulpinic acid, (+)-usnic acid, and (—)-usnic acid against aerobic and anaerobic microorganisms. Antimicrob. Agents Chemother. 39(11), 2541-2543 (1995).
2. Varol, M., TÜrk, A., Candan, M., et al. Photoprotective activity of vulpinic and gyrophoric acids toward ultraviolet B-induced damage in human keratinocytes. Phytother. Res. 30(1), 9-15 (2016).
3. Burlando, B., Ranzato, E., Volante, A., et al. Antiproliferative effects on tumour cells and promotion of keratinocyte wound healing by different lichen compounds. Planta. Med. 75(6), 607-613 (2009).
4. Sahin, E., Psav, S.D., Avan, I., et al. Vulpinic acid, a lichen metabolite, emerges as a potential drug candidate in the therapy of oxidative stress-related diseases, such as atherosclerosis. Hum. Exp. Toxicol. 38(6), 675-684 (2019).
| Cas No. | 521-52-8 | SDF | |
| 别名 | 吴耳酸 | ||
| Canonical SMILES | OC(/C(O1)=C(C(OC)=O)/C2=CC=CC=C2)=C(C3=CC=CC=C3)C1=O | ||
| 分子式 | C19H14O5 | 分子量 | 322.3 |
| 溶解度 | DMF: 30 mg/ml,DMF:PBS (pH 7.2) (1:2): 0.33 mg/ml,DMSO: 20 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 | 3.1027 mL | 15.5135 mL | 31.027 mL |
| 5 mM | 0.6205 mL | 3.1027 mL | 6.2054 mL |
| 10 mM | 0.3103 mL | 1.5513 mL | 3.1027 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。
Vulpinic Acid Controls Stem Cell Fate toward Osteogenesis and Adipogenesis
Genes (Basel) 2019 Dec 23;11(1):18.PMID:31878002DOI:10.3390/genes11010018.
Vulpinic Acid, a naturally occurring methyl ester of pulvinic acid, has been reported to exert anti-fungal, anti-cancer, and anti-oxidative effects. However, its metabolic action has not been implicated yet. Here, we show that Vulpinic Acid derived from a mushroom, Pulveroboletus ravenelii controls the cell fate of mesenchymal stem cells and preadipocytes by inducing the acetylation of histone H3 and α-tubulin, respectively. The treatment of 10T1/2 mesenchymal stem cells with Vulpinic Acid increased the expression of Wnt6, Wnt10a, and Wnt10b, which led to osteogenesis inhibiting the adipogenic lineage commitment, through the upregulation of H3 acetylation. By contrast, treatment with Vulpinic Acid promoted the terminal differentiation of 3T3-L1 preadipocytes into mature adipocytes. In this process, the increase in acetylated tubulin was accompanied, while acetylated H3 was not altered. As excessive generation of adipocytes occurs, the accumulation of lipid drops was not concentrated, but dispersed into a number of adipocytes. Consistently, the expressions of lipolytic genes were upregulated and inflammatory factors were downregulated in adipocytes exposed to Vulpinic Acid during adipogenesis. These findings reveal the multiple actions of Vulpinic Acid in two stages of differentiation, promoting the osteogenesis of mesenchymal stem cells and decreasing hypertrophic adipocytes, which can provide experimental evidence for the novel metabolic advantages of Vulpinic Acid.
The role of Vulpinic Acid as a natural compound in the regulation of breast cancer-associated miRNAs
Biol Res 2021 Nov 7;54(1):37.PMID:34743742DOI:10.1186/s40659-021-00360-4.
Background: Breast cancer is the most frequently diagnosed cancer, and no effective treatment solution has yet been found. The number of studies based on the research of novel natural compounds in the treatment of breast cancer has been increasing in recent years. The anticancer properties of natural compounds are related to the regulation of microRNA (miRNA) expression. Therefore, changing the profile of miRNAs with the use of natural products is very important in cancer treatment. However, the role of Vulpinic Acid and related miRNAs in breast cancer progression remains unknown. Vulpinic Acid, methyl (as2E)-2-(3-hydroxy-5-oxo-4-phenylfuran-2-ylidene)-2 phenylacetate, is a natural product extracted from the lichen species and shows an anticancer effect on different cancer cells. Methods: This study examines the effects of Vulpinic Acid on the miRNA levels of breast cancer (MCF-7) cells and its relationship with cell proliferation and apoptosis levels. The antiproliferative effect of Vulpinic Acid was screened against MCF-7 breast cancer cells and MCF-12A breast epithelial cells using the xCELLigence real-time cell analysis system. We analyzed the altered miRNA expression profile in MCF-7 breast cancer cells versus MCF-12A cells following their response to Vulpinic Acid through microarray analysis. The microarray analysis results were confirmed through quantitative real-time PCR and bioinformatics analysis. Results: The results of the miRNA array and bioinformatic analyses demonstrated that 12 miRNAs were specifically responsive to Vulpinic Acid in MCF-7 breast cancer cells. This is the first study to reveal that Vulpinic Acid inhibits the expression of 12 miRNAs and suppresses breast cancer cell proliferation. The study also revealed that Vulpinic Acid may downregulate the expression of 12 miRNAs by repressing the FOXO-3 gene. The miRNA targets were mainly found to play a role in the apoptosis, cell cycle and MAPK pathways. Moreover, Bcl-2, Bax, procaspase-3 and procaspase-9 protein levels were assessed by western blot analysis for validation of apoptosis at the protein level. Conclusion: This study revealed the molecular mechanisms of Vulpinic Acid on breast cancer and showed that Vulpinic Acid regulates apoptosis signaling pathways by decreasing the expression of miRNAs. The miRNA expression patterns illuminate the underlying effect of Vulpinic Acid in breast cancer treatment.
Vulpinic Acid, a lichen metabolite, emerges as a potential drug candidate in the therapy of oxidative stress-related diseases, such as atherosclerosis
Hum Exp Toxicol 2019 Jun;38(6):675-684.PMID:30868920DOI:10.1177/0960327119833745.
Vulpinic Acid, a lichen compound, has been shown to have many beneficial effects and its medicinal value increases day by day. As in atherosclerosis, endothelial damage is the basis of many diseases. The aim of this study is to investigate the effects of Vulpinic Acid against oxidative stress damage induced by hydrogen peroxide (H2O2) in endothelial cells. In order to find the IC50 of H2O2 and the protective dose of Vulpinic Acid, methyl thiazolyldiphenyl tetrazolium bromide (MTT) assays were performed. The amount of reactive oxygen species (ROS) induced by H2O2 and the protective effects of Vulpinic Acid against ROS were examined by fluorometric DCF-DA kit. The effects of H2O2 and Vulpinic Acid on actin filaments were determined by tetramethyl rhodamine (TRITC)-phalloidin fluorescence staining. Expression of Tie2 proteins was immunocytochemically analyzed in H2O2- and vulpinic acid-treated cells. After 24 h, the IC50 was found to be 215 μM in HUVECs treated with H2O2. The most effective dose of Vulpinic Acid against H2O2-associated damage was found to be 15 μM. Vulpinic Acid pretreatment was shown to reduce H2O2-induced ROS production significantly ( p < 0.05). It was shown that 215 μM of H2O2 caused actin fragmentation, cell shrinkage, and decrease in actin florescence intensity while Vulpinic Acid protected the cells from these damages. It was found that Tie2 immunoreactivity was decreased in H2O2-treated groups and Vulpinic Acid pretreatment reduced the expression of this protein. In conclusion, Vulpinic Acid decreases H2O2-induced oxidative stress and oxidative stress-related damages in HUVECs. It may be drug candidate in the therapy of atherosclerosis.
Vulpinic Acid as a natural compound inhibits the proliferation of metastatic prostate cancer cells by inducing apoptosis
Mol Biol Rep 2021 Aug;48(8):6025-6034.PMID:34331181DOI:10.1007/s11033-021-06605-5.
Background: Lichen secondary metabolites have drawn considerable attention in recent years due to the limitations of current treatment options. Vulpinic Acid (VA) obtained from Letharia vulpina lichen species exerts a remarkable cytotoxic effect on different cancer types. However, the therapeutic efficacy of VA in metastatic prostate cancer (mPC) cells has not been investigated. In the present study, we aimed to identify VA-mediated cytotoxicity in PC-3 mPC cells compared with control cells. Methods and results: After identifying the cytotoxic concentrations of VA, VA induced apoptosis was analyzed by Annexin V, cell cycle, acridine orange and propidium iodide staining and RT-PCR analysis. Our findings showed that VA significantly decreased the viability of PC-3 cells (p < 0.01) and caused a considerable early apoptotic effects through G0/G1 arrest, nuclear blebbing and the activation of particularly initiator caspases. Conclusions: Therefore, VA may be a potential treatment option for mPC patients. However, the underlying molecular mechanisms of VA-induced apoptosis with advanced analysis should be further investigated.
The molecular mechanisms of Vulpinic Acid induced programmed cell death in melanoma
Mol Biol Rep 2022 Sep;49(9):8273-8280.PMID:35960408DOI:10.1007/s11033-022-07619-3.
Backgrounds: Malignant melanoma is an aggressive skin tumor with a rapidly increasing incidence and there is not yet a successful treatment strategy. Vulpinic Acid (VA) is derived from secondary metabolites from lichen species. In the current study, we, for the first time, investigated the anti-cancer effects of VA and the underlying mechanism VA induced programmed cell death in melanoma. Methods: The anti-cancer effects of VA on melanoma cells were evaluated by the xCELLigence system, flow cytometry, caspase-3 activity and RT-PCR analysis. Results: Our results showed that VA had a strong anti-proliferative effect on A-375 melanoma cells without damaging human epidermal melanocyte cells. Additionally, VA promoted apoptotic cell death through G2/M arrest and the activation of both intrinsic and extrinsic apoptosis pathways according to the analysis of 88 genes associated with apoptosis by qRT-PCR. Conclusions: Our findings suggest that VA could become an alternative topical and transdermal treatment strategy in the treatment of maligned melanoma cancer. However, further investigations are needed to assess the underlying molecular mechanism of VA mediated apoptotic cell death in the treatment of melanoma.