3',4'-Dihydroxyflavonol
(Synonyms: 3,3',4'-三羟基黄酮,DiOHF) 目录号 : GC34451
3',4'-Dihydroxyflavonol(DiOHF)是一种有效的抗氧化剂，可降低糖尿病大鼠肠系膜动脉中的超氧化物并改善NO功能。
Cas No.:6068-78-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
3',4'-Dihydroxyflavonol (DiOHF) is an effective antioxidant, which reduces superoxide and improves nitric oxide (NO) function in diabetic rat mesenteric arteries[1].
3',4'-Dihydroxyflavonol (DiOHF) acutely preserves nitric oxide (NO) activity in the presence of elevated reactive oxygen species (ROS). DiOHF improves NO activity in diabetes by reducing Nox2-dependent superoxide production and preventing eNOS uncoupling to improve endothelial function[1].3',4'-Dihydroxyflavonol reduces vascular contraction through Ca²? desensitization in permeabilized third-order branches of rat mesenteric arteries[2].
[1]. Leo CH, et al. 3',4'-Dihydroxyflavonol reduces superoxide and improves nitric oxide function in diabetic rat mesenteric arteries. PLoS One. 2011;6(6):e20813. [2]. Kim HY, et al. 3',4'-Dihydroxyflavonol reduces vascular contraction through Ca²? desensitization in permeabilized rat mesenteric artery. Naunyn Schmiedebergs Arch Pharmacol. 2012 Feb;385(2):191-202.
| Cas No. | 6068-78-6 | SDF | |
| 别名 | 3,3',4'-三羟基黄酮,DiOHF | ||
| Canonical SMILES | O=C1C(O)=C(C2=CC=C(O)C(O)=C2)OC3=C1C=CC=C3 | ||
| 分子式 | C15H10O5 | 分子量 | 270.24 |
| 溶解度 | Soluble in DMSO | 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 | 3.7004 mL | 18.5021 mL | 37.0041 mL |
| 5 mM | 0.7401 mL | 3.7004 mL | 7.4008 mL |
| 10 mM | 0.37 mL | 1.8502 mL | 3.7004 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。
3', 4'-dihydroxyflavonol attenuates tissue damage in unilateral testis ischemia-reperfusion in rats
Bratisl Lek Listy 2015;116(12):735-40.PMID:26924144DOI:10.4149/bll_2015_144.
The purpose of this study was to determine the effect of 3',4'-Dihydroxyflavonol (DiOHF) on oxidative damage and antioxidant system in experimental testicular torsion-detorsion.The study included 60 male Wistar albino rats. Study groups were formed as follows: 1. Control; 2. Sham; 3. 720° - 4 hours torsion; 4. 720° - 4 hours torsion + 4 hours detorsion; 5. 720° - 4 hours torsion + DiOHF; 6. 720° - 4 hours torsion + DiOHF + 4 hours detorsion; 7. 720° - 4 hours torsion + 24 hours detorsion; 8. 720° - 4 hours torsion + DiOHF + 24 hours detorsion. Testis were collected for the analysis of glutathione peroxidase (GPx), nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), and xanthine oxidase (XO).GPx in the Group 8 were higher than the values in the other groups (p < 0.001). Concerning NO, the groups 3, 4, and 7 were found to have higher values than other groups (p < 0.001). MDA levels were higher in the groups 3, 7, and 8, when compared to the levels in other groups (p < 0.001). When tissue GSH levels were examined, the Group 5 had the highest GSH values (p < 0.001).With regard to XO values, the groups 3, 4, and 7 had the highest XO values (p < 0.001). The results of the study indicated that intraperitoneal DiOHF inhibited increased lipid peroxidation in testis ischemia-reperfusion injury in rats (Tab. 5, Ref. 46).
3',4'-Dihydroxyflavonol (DiOHF) prevents DNA damage, lipid peroxidation and inflammation in ovarian ischaemia-reperfusion injury of rats
J Obstet Gynaecol 2022 Feb;42(2):338-345.PMID:34159896DOI:10.1080/01443615.2021.1916813.
This study aimed to determine the effect of 3',4'-Dihydroxyflavonol (DiOHF) on lipid peroxidation, DNA damage and inflammation in ovarian ischaemia (I)-reperfusion (R) injury. This study was performed on 44 Wistar-albino female rats. Groups were designed as Control; Sham; I/R (the left ovary was ligated for 2 h and then reperfused for 2 h); I/R + DiOHF (after 2 h ischaemia and 2 h reperfusion, 30 mg/kg of DiOHF was given intraperitoneally and reperfusion was allowed for 2 h more); I + DiOHF + R (after 2 h I, 30 mg/kg of DiOHF was given at the beginning of 2 h reperfusion); DiOHF + I/R (2 h after DiOHF administration, the left ovary was ligated for 2 h and then reperfused for 2 h). Blood and ovarian tissue samples were analysed for GSH, MDA, 8-OHdG, SOD, and IL-6. Ovarian tissue was examined histopathologically. Ovarian I/R has led to inflammation and oxidative damage. However, DiOHF activated the antioxidant system and prevented DNA damage induced by I/R in ovarian tissue. Vascularisation, oedema, and inflammation also occurred in ovarian tissue in I/R group. The results of this study indicated that I/R led to disturbance of the oxidant/antioxidant system balance and increased DNA damage; however, DiOHF supplementation prevented DNA damage, lipid peroxidation and inflammation by increasing the antioxidant system in ovarian I/R injury in rats. However, in potential I/R situations, DiOHF application appears to be beneficial in reducing inflammation, oxidant injury, and DNA damage, and in activating the antioxidant system. IMPACT STATEMENTWhat is already known on this subject? Ischaemia/reperfusion (I/R) injuries lead to damage in cells or tissues due to insufficient blood flow.What do the results of this study add? Increased DNA injury and inflammatory response (IL-6) and structural impairment were treated by administration of intraperitoneal (DiOHF) which strongly stimulated the antioxidant system, inhibited antioxidant activities, prevented DNA damage and inflammation process.What are the implications of these findings for clinical practice and/or further research? This study's strength is that it is the first research demonstrates the prevention of DNA damage in ovarian I/R by DiOHF supplementation. This flavonoid (DiOHF) may be used for treatment in different ovarian ischaemia/reperfusion.
Inhibitory Effects of 3',4'-Dihydroxyflavonol in a Mouse Model of Glaucoma Filtration Surgery and TGFβ1-Induced Responses in Human Tenon's Fibroblasts
Transl Vis Sci Technol 2022 Aug 1;11(8):18.PMID:35980669DOI:10.1167/tvst.11.8.18.
Purpose: Cytotoxic agents such as mitomycin C (MMC) are part of the mainstay treatment for limiting subconjunctival scarring following glaucoma filtration surgery (GFS). However, a safer antifibrotic therapy is clinically needed. The anti-scarring properties of 3',4'-Dihydroxyflavonol (DiOHF) were evaluated in a mouse model of GFS and in cultured human Tenon's fibroblasts (HTFs). Methods: GFS was performed in C57BL/6 mice receiving daily intraperitoneal injections of DiOHF or vehicle or a single intraoperative injection of MMC. Eyes were harvested on day 14 for assessment of collagen deposition, expression of alpha-smooth muscle actin (α-SMA), cluster of differentiation 31 (CD31), and 4-hydroxy-2-nonenal (4HNE) in the conjunctiva/Tenon's layer. The inhibitory effects of DiOHF on transforming growth factor β (TGFβ)-induced responses were also assessed in HTFs. Results: Treatment with DiOHF demonstrated a reduction in collagen deposition at the GFS site compared to vehicle-treated mice. The degree of 4HNE-positive fluorescence was significantly reduced in DiOHF-treated eyes compared to the other groups, indicating a decrease in oxidative stress. A reduction in expression of α-SMA and CD31 was seen in DiOHF-treated conjunctiva compared to those treated with vehicle. Concordant results were demonstrated in cultured HTFs in vitro. Furthermore, treatment of cultured HTFs with DiOHF also displayed a reduction in the proliferation, migration, and contractility of HTFs. Conclusions: Treatment with DiOHF reduces scarring and angiogenesis in the conjunctiva of mice with GFS at a level comparable to MMC. The reduction in oxidative stress suggests that DiOHF may suppress scarring via different mechanisms from MMC. Translational relevance: DiOHF may be a safer and superior wound modulating agent than conventional antifibrotic therapy in GFS.
3',4'-Dihydroxyflavonol Modulates the Cell Cycle in Cancer Cells: Implication as a Potential Combination Drug in Osteosarcoma
Pharmaceuticals (Basel) 2021 Jul 3;14(7):640.PMID:34358066DOI:10.3390/ph14070640.
New agents are demanded to increase the therapeutic options for osteosarcoma (OS). Although OS is the most common bone cancer in children and adolescents, it is considered a rare disorder. Therefore, finding adjuvant drugs has potential to advance therapy for this disease. In this study, 3',4'-Dihydroxyflavonol (DiOHF) was investigated to assess the effects in OS cellular models in combination with doxorubicin (Dox). MG-63 and U2OS human OS cells were exposed to DiOHF and Dox and tested for cell viability and growth. To elucidate the inhibitory effects of DiOHF, additional studies were conducted to assess apoptosis and cell cycle distribution, gene expression quantification of cell cycle regulators, and cytokinesis-block cytome assay to determine nuclear division rate. DiOHF decreased OS cell growth and viability in a concentration-dependent manner. Its combination with Dox enabled Dox dose reduction in both cell lines, with synergistic interactions in U2OS cells. Although no significant apoptotic effects were detected at low concentrations, cytostatic effects were demonstrated in both cell lines. Incubation with DiOHF altered cell cycle dynamics and resulted in differential cyclin and cyclin-dependent kinase expression. Overall, this study presents an antiproliferative action of DiOHF in OS combination therapy via modulation of the cell cycle and nuclear division.
3',4'-Dihydroxyflavonol ameliorates endoplasmic reticulum stress-induced apoptosis and endothelial dysfunction in mice
Sci Rep 2018 Jan 29;8(1):1818.PMID:29379034DOI:10.1038/s41598-018-19584-8.
Endoplasmic reticulum (ER) stress has been implicated in the development of hypertension 3 through the induction of endothelial impairment. As 3',4'-Dihydroxyflavonol (DiOHF) 4 reduces vascular injury caused by ischaemia/reperfusion or diabetes, and flavonols have been demonstrated to attenuate ER stress, we investigated whether DiOHF can protect mice from ER stress-induced endothelial dysfunction. Male C57BLK/6 J mice were injected with tunicamycin to induce ER stress in the presence or absence of either DiOHF or tauroursodeoxycholic acid (TUDCA), an inhibitor of ER stress. Tunicamycin elevated blood pressure and impaired endothelium-dependent relaxation. Moreover, in aortae there was evidence of ER stress, oxidative stress and reduced NO production. This was coincident with increased NOX2 expression and reduced phosphorylation of endothelial nitric oxide synthase (eNOS) on Ser1176. Importantly, the effects of tunicamycin were significantly ameliorated by DiOHF or TUDCA. DiOHF also inhibited tunicamycin-induced ER stress and apoptosis in cultured human endothelial cells (HUVEC). These results provide evidence that ER stress is likely an important initiator of endothelial dysfunction through the induction of oxidative stress and a reduction in NO synthesis and that DiOHF directly protects against ER stress- induced injury. DiOHF may be useful to prevent ER and oxidative stress to preserve endothelial function, for example in hypertension.