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    Baohuoside I
    Information
    CAS No. 113558-15-9 Price $100 / 20mg
    Catalog No.CFN98525Purity>=98%
    Molecular Weight514.52Type of CompoundFlavonoids
    FormulaC27H30O10Physical DescriptionYellow powder
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    Baohuoside I

    Baohuoside I
    Product Name Baohuoside I
    CAS No.: 113558-15-9
    Catalog No.: CFN98525
    Molecular Formula: C27H30O10
    Molecular Weight: 514.52 g/mol
    Purity: >=98%
    Type of Compound: Flavonoids
    Physical Desc.: Yellow powder
    Targets: CXCR | Wnt/尾-catenin | ROS | Bcl-2/Bax | Caspase | JNK | p38MAPK
    Source: The roots of Epimedium brevicornu Maxim
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Price: $100 / 20mg
    Inquire / Order: manager@chemfaces.com
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  • Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
    10 mM * 1 mL in DMSO / Inquiry / In-stock
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  • Biological Activity
    Description: Baohuoside I is a novel immunosuppressive molecule, exhibits antimetastatic, anti-osteoporosis, anti-inflammatory and anti-cancer activities. Baohuoside I can inhibit the proliferation of Eca-109 cells, this effect associats with down-regulation expression of β-catenin,Cyclin D1,Survivin,and their proteins,which affects on the Wnt/β-catenin signaling pathway.
    Targets: CXCR | Wnt/β-catenin | ROS | Bcl-2/Bax | Caspase | JNK | p38MAPK
    In vitro:
    Chinese Traditional & Herbal Drugs, 2011, 42(1):124-6.
    Effect of baohuoside-I on Wnt/β-catenin signaling pathway of human esophageal carcinoma cell Eca-109.[Reference: WebLink]
    To study the effect of baohuoside-I extracted from Periplocae Cortex on proliferation and Wnt/β-catenin signaling pathway of human esophageal carcinoma cell Eca-109.
    METHODS AND RESULTS:
    The expressions of β-catenin, Cyclin D1, and Survivin protein in Eca-109 cells were measured with flow cytometry (FCM). The expressions of β-catenin, Cyclin D1, and Survivin mRNA were detected by RT-PCR. After treatment with 25 and 50 μg/mL of Baohuoside I for 48 h, the expression levels of β-catenin, Cyclin D1, Survivin mRNA, and protein were decreased significantly (P<0.01), but with 12.5 μg/ML of Baohuoside I the expression level was not decreased significantly compared with the control group.
    CONCLUSIONS:
    : Baohuoside I from Periplocae Cortex could inhibit the proliferation of Eca-109 cells. This effect associais with down-regulation expression of β-catenin, Cyclin D1, Survivin, and their proteins, which affects on the Wnt/β-catenin signaling pathway.
    Chem Biol Interact. 2012 Jul 30;199(1):9-17.
    Reactive oxygen species-mediated mitochondrial pathway is involved in Baohuoside I-induced apoptosis in human non-small cell lung cancer.[Pubmed: 22687635]
    Baohuoside I (also known as Icariside II) is a flavonoid isolated from Epimedium koreanum Nakai. Although Baohuoside I exhibits anti-inflammatory and anti-cancer activities, its molecular targets/pathways in human lung cancer cells are poorly understood. Therefore, in the present study, we investigated the usefulness of Baohuoside I as a potential apoptosis-inducing cytotoxic agent using human adenocarcinoma alveolar basal epithelial A549 cells as in vitro model.
    METHODS AND RESULTS:
    The apoptosis induced by Baohuoside I in A549 cells was confirmed by annexin V/propidium iodide double staining, cell cycle analysis and dUTP nick end labeling. Further research revealed that Baohuoside I accelerated apoptosis through the mitochondrial apoptotic pathway, involving the increment of BAX/Bcl-2 ratio, dissipation of mitochondrial membrane potential, transposition of cytochrome c, caspase 3 and caspase 9 activation, degradation of poly (ADP-ribose) polymerase and the over-production of reactive oxygen species (ROS). A pan-caspase inhibitor, Z-VAD-FMK, only partially prevented apoptosis induced by Baohuoside I, while NAC, a scavenger of ROS, diminished its effect more potently. In addition, the apoptotic effect of Baohuoside I was dependent on the activation of ROS downstream effectors, JNK and p38(MAPK), which could be almost abrogated by using inhibitors SB203580 (an inhibitor of p38(MAPK)) and SP600125 (an inhibitor of JNK).
    CONCLUSIONS:
    These findings suggested that Baohuoside I might exert its cytotoxic effect via the ROS/MAPK pathway.
    Transplantation. 2004 Sep 27;78(6):831-8.
    Baohuoside-1, a novel immunosuppressive molecule, inhibits lymphocyte activation in vitro and in vivo.[Pubmed: 15385801]
    We evaluated the in vitro and in vivo immunosuppressive effects of Baohuoside I (B1), a novel flavonoid isolated from Epimedium davidii.
    METHODS AND RESULTS:
    Proliferation assay was used to determine the antiproliferative properties on T-cell and B-cell proliferation. Flow cytometry analysis was applied to detect changes of phenotypes on activated cells. B1 inhibits the lymphocyte proliferation activated by polyclonal mitogens and mixed lymphocyte reaction with a 50% inhibitory concentration of low micromolar concentration. Also, B1 suppressed T-cell activation in T cell receptor/CD3-mediated signaling pathways in a dose- and time-dependent manner. The suppression of B1 was not simply a result of a toxic effect and was recovered by withdrawing the drug. B1 down-regulated the expression of some phenotype molecules. In Ca(2+)-independent or -dependent antigen stimulation, although B1 had different inhibitive patterns on CD69 expression stimulated by phorbol 12-myristate 13-acetate (PMA) or Ca2+ ionophore, it inhibited T-cell proliferation induced by CD3/CD28 or PMA/ionomycin and partially blocked that induced by PMA/CD28. Interestingly, an additive inhibition between B1 and tacrolimus (FK506) was found in the CD69 expression stimulated by PMA/CD28 and PMA/ionomycin. Similarly, this immunosuppression by combination therapy was observed in a heart transplantation model in vivo and might act through an immunosuppressive mechanism different from FK506.
    CONCLUSIONS:
    B1, whose mechanism of action is not similar to that of FK506, has selectively immunosuppressive effects on T-cell and B-cell activation in vitro and effectively prevents rat heart allograft rejection in vivo.
    Biochemistry . 2014 Dec 9;53(48):7562-9.
    Baohuoside I suppresses invasion of cervical and breast cancer cells through the downregulation of CXCR4 chemokine receptor expression[Pubmed: 25407882]
    Abstract More than 90 percent of cancer-mediated deaths are due to metastasis, but the mechanisms that control metastasis remain poorly understood. Thus, the therapy targeting this process has been challenged constantly, but no therapy has yet been approved. CXC chemokine receptor 4 (CXCR4), a Gi protein-coupled receptor for the CXC chemokine ligand (CXCL) 12/stromal cell derived factor (SDF) 1α, is known to be expressed in various tumors. Recently, the CXCL12/CXCR4 axis has emerged as a key mediator of tumor metastasis; therefore, the possibility that identification of CXCR4 inhibitors can be a promising strategy for abrogating metastasis has been considered. In this report, we investigate Baohuoside I, a component of Epimedium koreanum, as a regulator of CXCR4 expression as well as function in cervical cancer and breast cancer cells. We observed that Baohuoside I downregulated CXCR4 expression in a dose- and time-dependent manner in HeLa cells. Treatment with a pharmacological proteasome and lysosomal inhibitors did not have a substantial effect on Baohuoside I's ability to suppress CXCR4 expression. When we investigated the molecular mechanism of action, it was observed that the suppression of CXCR4 expression occurred at the level of mRNA. The decrease in the level of CXCR4 expression caused by Baohuoside I was correlated with inhibition of the CXCL12-induced invasion of both cervical and breast cancer cells. Overall, our results show that Baohuoside I exerts its antimetastatic effect through the downregulation of CXCR4 expression and, thus, has the potential to play a role in the suppression of cancer metastasis.
    Baohuoside I Description
    Source: The roots of Epimedium brevicornu Maxim
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.9436 mL 9.7178 mL 19.4356 mL 38.8712 mL 48.589 mL
    5 mM 0.3887 mL 1.9436 mL 3.8871 mL 7.7742 mL 9.7178 mL
    10 mM 0.1944 mL 0.9718 mL 1.9436 mL 3.8871 mL 4.8589 mL
    50 mM 0.0389 mL 0.1944 mL 0.3887 mL 0.7774 mL 0.9718 mL
    100 mM 0.0194 mL 0.0972 mL 0.1944 mL 0.3887 mL 0.4859 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Kinase Assay:
    Biochemistry. 2014 Dec 9;53(48):7562-9.
    Baohuoside I suppresses invasion of cervical and breast cancer cells through the downregulation of CXCR4 chemokine receptor expression.[Pubmed: 25407882]
    More than 90 percent of cancer-mediated deaths are due to metastasis, but the mechanisms that control metastasis remain poorly understood. Thus, the therapy targeting this process has been challenged constantly, but no therapy has yet been approved. CXC chemokine receptor 4 (CXCR4), a Gi protein-coupled receptor for the CXC chemokine ligand (CXCL) 12/stromal cell derived factor (SDF) 1α, is known to be expressed in various tumors. Recently, the CXCL12/CXCR4 axis has emerged as a key mediator of tumor metastasis; therefore, the possibility that identification of CXCR4 inhibitors can be a promising strategy for abrogating metastasis has been considered.
    METHODS AND RESULTS:
    In this report, we investigate Baohuoside I, a component of Epimedium koreanum, as a regulator of CXCR4 expression as well as function in cervical cancer and breast cancer cells. We observed that Baohuoside I downregulated CXCR4 expression in a dose- and time-dependent manner in HeLa cells. Treatment with a pharmacological proteasome and lysosomal inhibitors did not have a substantial effect on Baohuoside I's ability to suppress CXCR4 expression. When we investigated the molecular mechanism of action, it was observed that the suppression of CXCR4 expression occurred at the level of mRNA. The decrease in the level of CXCR4 expression caused by Baohuoside I was correlated with inhibition of the CXCL12-induced invasion of both cervical and breast cancer cells.
    CONCLUSIONS:
    Overall, our results show that Baohuoside I exerts its antimetastatic effect through the downregulation of CXCR4 expression and, thus, has the potential to play a role in the suppression of cancer metastasis.
    Cell Research:
    Oncol Rep. 2011 Nov;26(5):1149-56.
    The flavonoid Baohuoside-I inhibits cell growth and downregulates survivin and cyclin D1 expression in esophageal carcinoma via β-catenin-dependent signaling.[Pubmed: 21785828]
    Esophageal cancer is one of the most common malignancies and is associated with a dismal prognosis. Although treatment options have increased for some patients, overall progress has been modest. Thus, there is a great need to develop new treatments. We found that Baohuoside I, a flavonoid extracted from a Chinese medicinal plant, exhibits anticancer activity.
    METHODS AND RESULTS:
    Here, we demonstrated that Baohuoside I significantly inhibited Eca109 human esophageal squamous carcinoma cell proliferation and induced Eca109 cell apoptosis in vitro and in vivo. The growth inhibitory effect of Baohuoside-I on the Eca109 tumor cell line was examined by MTT assay; the induction of apoptosis was analyzed by flow cytometry. Eca109-luc cells were injected into the subcutaneous tissue of nude mice to establish xenograft tumors. Our results revealed that Baohuoside-I caused a dose- and time-dependent inhibition of cell growth and an induction of apoptosis. Furthermore, Baohuoside I-treated cells were characterized by decreased expression of the β-catenin gene and protein in the total cell lysates. Thus, the gene and protein expression of the downstream elements survivin and cyclin D1 was downregulated. To determine the precise inhibitory mechanisms involved, further in-depth in vivo studies of Baohuoside I are warranted.
    CONCLUSIONS:
    Our study provides the first evidence that Baohuoside I inhibits tumor growth and induces apoptosis by inhibiting β-catenin-dependent signaling pathways. Thus, Baohuoside I is a potential candidate in ESCC disease therapy.
    Animal Research:
    Yao Xue Xue Bao. 2014 Jun;49(6):932-7.
    Two-dimensional zebrafish model combined with hyphenated chromatographic techniques for evaluation anti-osteoporosis activity of epimendin A and its metabolite baohuoside I.[Pubmed: 25212043]
    This article firstly established a new efficient method for screening anti-osteoporosis ingredients, which used two-dimensional zebrafish model combined with hyphenated chromatographic techniques to evaluate anti-osteoporosis activities of epimedin A and its metabolite Baohuoside I.
    METHODS AND RESULTS:
    Adult zebrafish was used for metabolism of epimedin A in 0.5% DMSO, and LC-MS was used for analysis of the metabolite, which was captured by HPLC, and prednisolone-induced osteoporosis model of zebrafish was used to evaluate the anti-osteoporotic activities of trace amounts of epimedin A and Baohuoside I. The results indicated that epimedin A and Baohuoside I can prevent prednisolone-induced osteoporosis in zebrafish. The developed method in this paper enables the separation, enrichment and analysis of micro-amount metabolite of epimedin A, and anti-osteoporosis activities in vivo of epimedin A and Baohuoside I was simple and efficient screening resorting to zebrafish osteoporosis mode.
    CONCLUSIONS:
    This paper would provide new ideas and methods for a rapid and early discovery of anti-osteoporosis activities of micro-ingredients and its metabolite of traditional Chinese medicine.
    Baohuoside I References Information
    Citation [1]

    Carcinogen.Teratogen. Mut., 2011, 23(5):367-9.

    Effects of Baohuoside-I and 5-FU on the proliferation and apoptosis of human esophageal carcinoma cell Eca-109.[Reference: WebLink]
    To study the effects of Baohuoside I in combination with 5-FU on the proliferation and apoptosis of human esophageal carcinoma cell Eca-109. METHODS:The cells were divided into 4 groups: combination group (12.5 mg/L Baohuoside I and 12.5 mg/L 5-FU),negative control group (0.1% DMSO),25 mg/L Baohuoside I group and 12.5 mg/L 5-FU group,with 3 holes in each group and 100 μl each hole (1×104 cells ). After treatment for 24,48,72 h,the inhibitory effect on proliferation of Eca-109 cells was analyzed by MTT. After treatment for 48 h,apoptosis of Eca-109 cells was measured with flow cytometry;the expression of Bcl-2 protein and Bax protein of Eca-109 cells was measured with Western blot. RESULTS:Baohuoside I,5-FU alone and Baohuoside I in combination with 5-FU inhibited proliferation of Eca-109 cells (P all <0.05),the inhibitory effect of the combination group was superior to either alone (P <0.05). After treatment for 48 h,apoptosis of Eca-109 cells was induced significantly,the expression of Bcl-2 protein was decreased and Bax protein was increased significantly than control group (P all <0.05). T he combination group showed more significant effect than either alone (P <0.05). CONCLUSION: Baohuoside I in combination with 5-FU exerted a synergistic effect on inhibiting proliferation and promoting apoptosis. This effect associated with decreased expression of Bcl-2 and increased expression of Bax.
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