Skullcapflavone II
(Synonyms: 黄芩黄酮II) 目录号 : GC60340
SkullcapflavoneII是从黄芩中提取的黄酮类化合物，具有抗炎、抗菌作用。SkullcapflavoneII调节破骨细胞的分化、存活和功能。SkullcapflavoneII对M.aurum和M.bovisBCG具有较强的抗菌活性。
Cas No.:55084-08-7
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
Skullcapflavone II, a flavonoid derived from Scutellaria baicalensis, has anti-inflammatory, anti-microbial activities. Skullcapflavone II regulates osteoclast differentiation, survival, and function. Skullcapflavone II exerts potent antimicrobial activity against M. aurum and M. bovis BCG[1][2].
Skullcapflavone II inhibits osteoclastogenesis with decreased activation of MAPKs, Src, and cAMP response element-binding protein (CREB), which have been known to be redox sensitive. Skullcapflavone II decreases reactive oxygen species by scavenging them or activating nuclear factor-erythroid 2-related factor 2 (Nrf2), and its effects were partially reversed by hydrogen peroxide cotreatment or Nrf2 deficiency[2].
Skullcapflavone II, a potential bradykinin antagonist, reduces the major pathophysiological features of allergic asthma, at least in part by acting on TGF-β1/Smad signaling pathways[3].
[1]. Solnier J, et al. Flavonoids as Novel Efflux Pump Inhibitors and Antimicrobials Against Both Environmental and Pathogenic Intracellular Mycobacterial Species. Molecules. 2020;25(3):734. Published 2020 Feb 7. [2]. Lee J, et al. Skullcapflavone II inhibits osteoclastogenesis by regulating reactive oxygen species and attenuates the survival and resorption function of osteoclasts by modulating integrin signaling. FASEB J. 2019;33(2):2026-2036. [3]. Jang HY, et al. Skullcapflavone II inhibits ovalbumin-induced airway inflammation in a mouse model of asthma [published correction appears in Int Immunopharmacol. 2013 Sep;17(1):154]. Int Immunopharmacol. 2012;12(4):666-674.
| Cas No. | 55084-08-7 | SDF | |
| 别名 | 黄芩黄酮II | ||
| Canonical SMILES | COC1=C2C(C(C=C(C3=C(C=CC=C3O)OC)O2)=O)=C(O)C(OC)=C1OC | ||
| 分子式 | C19H18O8 | 分子量 | 374.34 |
| 溶解度 | 储存条件 | ||
| 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 | 2.6714 mL | 13.3568 mL | 26.7137 mL |
| 5 mM | 0.5343 mL | 2.6714 mL | 5.3427 mL |
| 10 mM | 0.2671 mL | 1.3357 mL | 2.6714 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。
Skullcapflavone II Suppresses TNF-α/IFN-γ-Induced TARC, MDC, and CTSS Production in HaCaT Cells
Int J Mol Sci 2021 Jun 16;22(12):6428.PMID:34208434DOI:10.3390/ijms22126428.
Skullcapflavone II (SFII), a flavonoid derived from Scutellaria baicalensis, has been reported to have anti-inflammatory properties. However, its therapeutic potential for skin inflammatory diseases and its mechanism are unknown. Therefore, this study aimed to investigate the effect of SFII on TNF-α/IFN-γ-induced atopic dermatitis (AD)-associated cytokines, such as thymus- and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC). Co-stimulation with TNF-α/IFN-γ in HaCaT cells is a well-established model for induction of pro-inflammatory cytokines. We treated cells with SFII prior to TNF-α/IFN-γ-stimulation and confirmed that it significantly inhibited TARC and MDC expression at the mRNA and protein levels. Additionally, SFII also inhibited the expression of cathepsin S (CTSS), which is associated with itching in patients with AD. Using specific inhibitors, we demonstrated that STAT1, NF-κB, and p38 MAPK mediate TNF-α/IFN-γ-induced TARC and MDC, as well as CTSS expression. Finally, we confirmed that SFII significantly suppressed TNF-α/IFN-γ-induced phosphorylation of STAT1, NF-κB, and p38 MAPK. Taken together, our study indicates that SFII inhibits TNF-α/IFN-γ-induced TARC, MDC, and CTSS expression by regulating STAT1, NF-κB, and p38 MAPK signaling pathways.
Skullcapflavone II Inhibits Degradation of Type I Collagen by Suppressing MMP-1 Transcription in Human Skin Fibroblasts
Int J Mol Sci 2019 Jun 4;20(11):2734.PMID:31167359DOI:10.3390/ijms20112734.
Skullcapflavone II is a flavonoid derived from the root of Scutellaria baicalensis, a herbal medicine used for anti-inflammatory and anti-cancer therapies. We analyzed the effect of Skullcapflavone II on the expression of matrix metalloproteinase-1 (MMP-1) and integrity of type I collagen in foreskin fibroblasts. Skullcapflavone II did not affect the secretion of type I collagen but reduced the secretion of MMP-1 in a dose- and time-dependent manner. Real-time reverse transcription-PCR and reporter gene assays showed that Skullcapflavone II reduced MMP-1 expression at the transcriptional level. Skullcapflavone II inhibited the serum-induced activation of the extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways required for MMP-1 transactivation. Skullcapflavone II also reduced tumor necrosis factor (TNF)-α-induced nuclear factor kappa light chain enhancer of activated B cells (NF-κB) activation and subsequent MMP-1 expression. In three-dimensional culture of fibroblasts, Skullcapflavone II down-regulated TNF-α-induced MMP-1 secretion and reduced breakdown of type I collagen. These results indicate that Skullcapflavone II is a novel biomolecule that down-regulates MMP-1 expression in foreskin fibroblasts and therefore could be useful in therapies for maintaining the integrity of extracellular matrix.
Skullcapflavone II protects neuronal damage in cerebral ischemic rats via inhibiting NF-ĸB and promoting angiogenesis
Microvasc Res 2022 May;141:104318.PMID:35026288DOI:10.1016/j.mvr.2022.104318.
Background: Cerebral ischemia (CI) is considered as a main cause of cerebral stroke (CS) and poses significant risk to the mankind across the world. In the present study, we intended to investigate the protective effect of Skullcapflavone II (SCP) a flavonoid isolated from S. baicalensis on cerebral ischemia/reperfusion (I/R) injury. Methods: The middle cerebral artery occlusion (MCAO) and reperfusion was used to create ischemic stroke rat model. The rats were treated with (5, 10, and 15 mg/kg) SCP and after the end of the experiment the rats were sacrificed and various biochemical parameters were assed to determine the pharmacological action of SCP. Results: SCP dramatically decreases cerebral edema, infarct volume, and improves neurological manifestation as confirmed by reduced neurological deficit. SCP also improves the survivability of neurons as evidenced by H and E and Nissl staining. The level of oxidative stress in the cerebral cortex of the rats was found reduced after treatment with SCP, as confirmed by increase in GSH and SOD activity with reduction in MDA content. In addition, SCP attenuated inflammation via reducing the level of TNF-α, IL-1β and IL-6 in brain tissues of rats. SCP increases the expression of Bcl2, cleaved caspase-3 and -9, while decreasing Bax, and NF-ĸB/TLR4. It causes induction of angiogenesis as suggested by increased expression of VEGF, Ang-1 and Tie-2 in cerebral cortex of rat. Conclusions: Our data determined that SCP may provide protective effect on the I/R-induced cerebral ischemia.
Skullcapflavone II inhibits ovalbumin-induced airway inflammation in a mouse model of asthma
Int Immunopharmacol 2012 Apr;12(4):666-74.PMID:22314230DOI:10.1016/j.intimp.2012.01.010.
Skullcapflavone II is a flavonoid derived from Scutellaria baicalensis, a widely used herbal medicine in anti-inflammatory and anticancer therapy in Korea. Skullcapflavone II antagonized the bradykinin receptor more potently than any of the other flavonoids derived from this plant. Here, we were investigated its therapeutic effects in a mouse model of ovalbumin (OVA)-induced allergic asthma. Administration of Skullcapflavone II significantly reduced airway hyperresponsiveness (AHR), airway eosinophilia, Th2 cytokine production, and increased transforming growth factor-β1 (TGF-β1) levels in bronchoalveolarlavage (BAL) fluids and lungs from OVA-sensitized and -challenged mice. Skullcapflavone II administration also significantly suppressed subepithelial collagen deposition and goblet cell hyperplasia, elevated Smad7 expression and suppressed pSmad2/3 levels. Collectively, these findings indicate that Skullcapflavone II, a potential bradykinin antagonist, reduced the major pathophysiological features of allergic asthma, at least in part by acting on TGF-β1/Smad signaling pathways. Thus, Skullcapflavone II may have therapeutic potential for the treatment of allergic asthma.
Topical Skullcapflavone II attenuates atopic dermatitis in a mouse model by directly inhibiting associated cytokines in different cell types
Front Immunol 2022 Dec 20;13:1064515.PMID:36605189DOI:10.3389/fimmu.2022.1064515.
Skullcapflavone II (SFII), a flavonoid derived from Scutellaria baicalensis, is an anticancer agent. We aimed to validate SFII for atopic dermatitis (AD) therapy by demonstrating the anti-inflammatory effects of SFII in an AD mouse model produced by the topical application of the vitamin D3 analog MC903. We showed that topical treatment with SFII significantly suppressed MC903-induced serum IgE levels compared with topical hydrocortisone (HC) treatment. Topical SFII also prevents MC903-induced pruritus, skin hyperplasia, and inflammatory immune cell infiltration into lesional skin comparable to topical HC. In addition, MC903-induced immune cell chemoattractants and AD-associated cytokine production in skin lesions were effectively suppressed by topical SFII. The production of MC903-induced effector cytokines influencing T helper (Th)2 and Th17 polarization in lesioned skin is significantly inhibited by topical SFII. Furthermore, we showed that SFII can directly inhibit the production of AD-associated cytokines by human primary keratinocytes, mouse bone marrow-derived cells (BMDCs), and mouse CD4+ T cells in vitro. Lastly, we demonstrated that topical SFII more effectively suppressed serum IgE levels, the production of IL-4 and thymic stromal lymphopoietin (TSLP), and infiltration of CD4+ T cells and Gr-1+ cells (neutrophils) into lesion skin compared to topical baicalein (a flavonoid derived from Scutellaria baicalensis), which has anti-inflammatory effects. Taken together, our findings suggest that SFII may have promising therapeutic potential for this complex disease via the regulation of multiple AD-associated targets.