Baohuoside I
(Synonyms: 宝藿苷 I; Icariin-II; Icariside-II) 目录号 : GN10507
A flavonoid with diverse biological activities
Cas No.:113558-15-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
Human cervical cancer HeLa cells |
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Preparation Method |
Baohuoside I was dissolved in dimethyl sulfoxide (DMSO) as a 10 mM stock solution and stored at 4℃. |
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Reaction Conditions |
Invasion assay by polycarbonate membranes with a pore size of 8 μm，25 μM baohuoside I |
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Applications |
Baohuoside I correlates with cervical cancer cell downregulation of CXC chemokine receptor 4. CXCL12 induced the invasion of cervical cancer cells, and baohuoside I effectively abrogated it. |
| Animal experiment [2]: | |
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Animal models |
Inbred female C57/BL/6J mice |
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Preparation Method |
Baohuoside I is stored in pure ethanol and suspended in 0.9% sterile saline intraperitoneal injection. |
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Dosage form |
Intraperitoneal injection, 20 mg/kg/d |
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Applications |
Mice received Baohuoside I by daily i.p. injection from day 0 to day 4. They were immunized with sheep red blood cells (SRBC) at day 0 and bled at day 5. The results showed significant suppression of anti-SRBC antibody responses at dosage schedules of 18.8 mg/ kg/day and above (P<0.001). |
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References: [1]. Kim B, et al. Baohuoside I suppresses invasion of cervical and breast cancer cells through the downregulation of CXCR4 chemokine receptor expression. Biochemistry. 2014 Dec 9;53(48):7562-9. [2]. Li SY, Ping G, Geng L, et al. Immunopharmacology and toxicology of the plant flavonoid baohuoside-1 in mice. Int J Immunopharmacol 1994; 16: 227. |
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Baohuoside I, a flavonoid isolated from Epimedium koreanum Nakai, acts as an inhibitor of CXCR4, downregulates CXCR4 expression, induces apoptosis and shows anti-tumor activity [1].
Baohuoside I exhibited strong inhibition against the α-glucosidase while icariin and epimedin A, B and C were weak or inactive. All compounds were inactive against pancreatic α-amylase. The IC50 of baohuoside I was 28.9 μmol/L[2].A549 cells were evidently inhibited by Baohuoside I in a time- and concentration-dependent manner. IC50 was approximately 25.1 μM at 24 h, 11.5μM at 48 h and 9.6μM at 72 h, respectively [3].
Baohuoside I prolonged graft survival on rat. A negative control group showed a mean survival time of 6.5±0.5 days. Monotherapy with a subtherapeutic oral dose of Baohuoside I (8.0 mg/kg/day) or FK506 (1.0 mg/kg/day) significantly prolonged cardiac allograft survival up to 9.0±2.0 days or 16.4±6.3 days, compared with negative controls. Results with combination therapy of these two drugs in the same doses (25.0±2.0 days) indicate that an additive prolongation of graft survival was produced when compared with monotherapy with Baohuoside I or FK506[4].
References:
[1]. Kim B, et al. Baohuoside I suppresses invasion of cervical and breast cancer cells through the downregulation of CXCR4 chemokine receptor expression. Biochemistry. 2014 Dec 9;53(48):7562-9.
[2]. M.A.T. Phan, J. Wang, J.Y. Tang, et al. Evaluation of α-glucosidase inhibition potential of some flavonoids from Epimedium brevicornum L. WT-Food Science and Technology, 53 (2013), pp. 492-498.
[3]. Song J, et al. Reactive oxygen species-mediated mitochondrial pathway is involved in Baohuoside I-induced apoptosis in human non-small cell lung cancer. Chem Biol Interact. 2012 Jul 30;199(1):9-17.
[4].A. Ma, S. Qi, D. Xu, X. Zhang, P. Daloze, H. Chen . Baohuoside-1, a novel immunosuppressive molecule, inhibits lymphocyte activation in vitro and in vivo. Transplantation, 78 (2004), pp. 831-838.
宝活苷 I 是一种从淫羊藿中分离出来的黄酮类化合物，可作为 CXCR4 抑制剂，下调 CXCR4 表达，诱导细胞凋亡并具有抗肿瘤活性[1]。
宝霍苷 I 对 α-葡萄糖苷酶表现出强烈的抑制作用，而淫羊藿苷和淫羊藿苷 A、B 和 C 则较弱或无活性。所有化合物均对胰腺 α-淀粉酶无活性。保活苷I的IC50为28.9 μmol/L[2]。保活苷I对A549细胞有明显的抑制作用，并呈时间和浓度依赖性。 IC50 在 24 小时时约为 25.1 μM，在 48 小时时约为 11.5 μM，在 72 小时时约为 9.6 μM [3]。
保活苷 I 延长了大鼠移植物的存活时间。阴性对照组显示平均存活时间为 6.5±0.5 天。与阴性对照相比，口服亚治疗剂量的宝活苷 I (8.0 mg/kg/天) 或 FK506 (1.0 mg/kg/天) 的单一疗法可显着延长心脏同种异体移植物的存活时间，达 9.0±2.0 天或 16.4±6.3 天。这两种药物以相同剂量（25.0±2.0 天）联合治疗的结果表明，与保活苷 I 或 FK506 的单药治疗相比，移植物存活时间得到额外延长[4]。
| Cas No. | 113558-15-9 | SDF | |
| 别名 | 宝藿苷 I; Icariin-II; Icariside-II | ||
| 化学名 | 5,7-dihydroxy-2-(4-methoxyphenyl)-8-(3-methylbut-2-enyl)-3-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxychromen-4-one | ||
| Canonical SMILES | CC1C(C(C(C(O1)OC2=C(OC3=C(C2=O)C(=CC(=C3CC=C(C)C)O)O)C4=CC=C(C=C4)OC)O)O)O | ||
| 分子式 | C27H30O10 | 分子量 | 514.18 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 10 mg/ml,Ethanol: 0.5 mg/ml,PBS (pH 7.2): 0.1 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 | 1.9448 mL | 9.7242 mL | 19.4484 mL |
| 5 mM | 0.389 mL | 1.9448 mL | 3.8897 mL |
| 10 mM | 0.1945 mL | 0.9724 mL | 1.9448 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。
Baohuoside I via mTOR Apoptotic Signaling to Inhibit Glioma Cell Growth
Cancer Manag Res2020 Nov 10;12:11435-11444.PMID: 33204156DOI: 10.2147/CMAR.S265803
Introduction: Baohuoside I, a novel oncotherapeutic agent, has been reported to have anti-cancer effects on a variety of cancers, but its role in glioma and its molecular mechanism are still unclear.
Methods: The proliferation of U251 cells was detected by real-time cellular analysis (RTCA), CCK-8, Ki67 immunofluorescence and colony formation assay. The effect of Baohuoside I on the invasion and migration of U251 cells was measured by transwell and scratch tests. The apoptosis of U251 cells was detected by flow cytometry. The expression level of related protein was detected by western blotting.
Results: Baohuoside I could inhibit the proliferation of human glioma cells and induce apoptosis. Further study showed that the migration and invasion ability of glioma was significantly decreased by Baohuoside I. Western blot revealed the expression of p-AMPKα1 protein was up-regulated, and the expression of p-mTOR and p-S6K was down-regulated after Baohuoside I treatment. Tumorigenesis in nude mice showed that Baohuoside I had an anti-glioma effect in vivo.
Conclusion: We propose a natural product, which can inhibit the proliferation, invasion and migration of glioma and may be a valuable anti-tumor candidate. The inhibitory effect of Baohuoside I on the glioma is achieved by inducing the apoptosis of the tumor cells, rather than autophagy. In addition, the pathway to induce cell apoptosis of Baohuoside I is to target the mTOR signal.
Baohuoside I Inhibits the Proliferation of Hepatocellular Carcinoma Cells via Apoptosis Signaling and NF-kB Pathway
Chem Biodivers2021 Jun;18(6):e2100063.PMID: 33904248DOI: 10.1002/cbdv.202100063
Baohuoside I is a flavonoid isolated from Epimedium koreanum Nakai and has many pharmacological activities. However, its role in liver cancer remains unclear. This study aimed to investigate the inhibitory effect of Baohuoside I on the Human Hepatocellular Carcinoma (HCC) cell lines QGY7703, and underlying mechanisms. QGY7703 cells were used as the model to assess the function of Baohuoside I in vitro. The effects of Baohuoside I on QGY7703 cells' growth, proliferation, and invasiveness were confirmed by CCK-8, lactate dehydrogenase release, and invasion assays. Cell apoptosis was analyzed by flow cytometry, and the levels of cleaved Caspase-3, Bax, and Bcl-2 were quantified by western blot. Western blot analysis, nuclear translocation of NF-κB, and Q-PCR were used to measure the expression of affected molecules. In QGY7703 cells, Baohuoside I induced the expression of molecules related to NF-κB pathway. The toxicity of Baohuoside I on QGY7703 cells was also confirmed in vivo, in a tumor model. Baohuoside I had a significant toxic effect on QGY7703 cells from a concentration of 10 μM. This compound significantly inhibited the proliferation of QGY7703 cells by inducing apoptosis and downregulating NF-κB signaling pathway. Thus, Baohuoside I is a novel candidate drug and opens new possibilities of clinical strategies for HCC treatment.
Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling
Cancer Manag Res2019 Dec 19;11:10609-10621.PMID: 31908533DOI: 10.2147/CMAR.S228926
Background: Although the incidence of pancreatic cancer has increased markedly, the 5-year survival rate for this disease is considerably low compared with other types of cancer. Moreover, the mortality rate of pancreatic cancer is similar to its incidence rate. Current therapeutic agents exhibit a lack of specificity for pancreatic cancer. Baohuoside I is traditionally used to treat orgasmic disorder and inflammation. However, its role in pancreatic cancer is unknown.
Objective: To explore the effects of Baohuoside I on pancreatic cancer and to study the potential-related molecular mechanism.
Materials and methods: In the present study, the antineoplastic effect of Baohuoside I was investigated with regard to pancreatic cancer via colony formation, transwell and migration assay. The energy metabolism changes of pancreatic cancer were tested by flow cytometry analysis and oxidative phosphorylation and glycolysis assay. The target signaling members were analyzed by Western blot.
Results: Baohuoside I inhibited the cell growth of pancreatic cancer cells. In addition, it affected intracellular energy metabolism to induce cancer cell apoptosis via the mTOR/S6K1 and the caspase/Bcl2/Bax signaling pathways.
Conclusion: The present data provide further insight into the development of novel drugs against pancreatic cancer.