Vitexin
(Synonyms: 牡荆素,Apigenin 8-C-glucoside; Vitexina; 4H-1-Benzopyran-4-one, 8-β-D-glucopyranosyl-5,7-dihydroxy-2-(4-hydroxyphenyl)-) 目录号 : GN10806
Vitexin is an active components of many traditional Chinese medicines, and were found in various medicinal plants.
Cas No.:3681-93-4
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 oral cancer cell line (OC2) |
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Preparation Method |
A total of 1000 cells were seeded in a 96-well plate for 24 h before treatment with vitexin (0, 12.5, 25, 50, 100 µM). At the end of incubation, add alamarBlue reagent in an amount equal to 10% of the volume in the well. Cultures were incubated for 4 h, and then cytotoxicty was measured by using spectrophotometry at 570 and 600 nm. |
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Reaction Conditions |
0, 12.5, 25, 50, 100 µM for for 48 h. |
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Applications |
Increasing concentration of vitexin drastic decreased cell viability of OC2 cells. |
| Animal experiment [2]: | |
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Animal models |
male adult Sprague-Dawley (SD) rats |
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Preparation Method |
rats were randomly divided into the following six groups with 16 rats in each group: (1) sham group, sham-operated without occludes the artery, (2) I/R group, I/R alone with normal saline (NS) treatment, (3) I/R + puerarin group, puerarin was administered intravenously at a dose of 30 mg/kg, beginning at coronary ischemia and again at reperfusion, (4) I/R + vitexin 6 mg/kg group, vitexin was administered intravenously at a dose of 6 mg/kg, beginning at coronary ischemia and again at reperfusion, (5) I/R + vitexin 3 mg/kg group, vitexin was administered intravenously at a dose of 3 mg/kg, beginning at coronary ischemia and again at reperfusion, (6) I/R + vitexin 1.5 mg/kg group, vitexin was administered intravenously at a dose of 1.5 mg/kg, beginning at coronary ischemia and again at reperfusion. |
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Dosage form |
Intravenous injection, 1.5, 3, 6 mg/kg |
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Applications |
The elevation of the ST segment was significantly enhanced in I/R group 30 min after ischemia, 30 and 60 min after reperfusion compared with sham group. Vitexin 6 mg/kg and puerarin have a significant inhibiting effect against the elevation of the ST segment 30 and 60 min after reperfusion compared with I/R group. |
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References: [1]: Yang S H, Liao P H, Pan Y F, et al. The novel p53‐dependent metastatic and apoptotic pathway induced by vitexin in human oral cancer OC2 cells[J]. Phytotherapy Research, 2013, 27(8): 1154-1161. | |
Vitexin is an active components of many traditional Chinese medicines, and were found in various medicinal plants. Vitexin (apigenin-8-C-glucoside) has recently received increased attention due to its wide range of pharmacological effects, including but not limited to anti-oxidant, anti-cancer, anti-inflammatory, anti-hyperalgesic, and neuroprotective effects [1]. vitexin has recently received increased attention due to its wide range of pharmacological effects, including anti-cancer, anti-oxidant, anti-inflammatory, anti-nociceptive, anti-AD (AD, Alzheimer's disease), anti-hypertensive, anti-spasmodic, anti-hypoxia/ischemia injury, anti-depressant-like actions and anti-viral activities [1].
Vitexin (20 µM, 24h) significantly reduced the HIF-1α level in rat pheochromocytoma PC12 cells, not in human hepatocellular carcinoma HepG2 or in human osteosarcoma HOS cells under hypoxia [2]. Vitexin reduced the levels of VEGF (the major angiogenic factor) protein and mRNA in a dose-dependent manner [2]. 20 µM of vitexin inhibited PC12 cells invasion by approximately 66% [2]. Vitexin-induced (100 µM, 48h) apoptosis was p53 dependent in human oral cancer OC2 cells [3]. Vitexin (100 µM, 48h) induced the expression of ERK 1/2 in OC2 cells [3].
Vitexin (40 mg/kg i.g.) increased the brain weights of D-galactose-aged mice [4]. vitexin (10-40 mg/kg i.g.) increased the activity of the antioxidase system and levels of ATPase in the serum and tissue of D-galactose-aged mice [4]. Vitexin (0.3-10 mg/kg, i.p.) inhibits the mice writhing response induced by acetic acid and phenyl-p-benzoquinone (PBQ) [5]. Vitexin (1-10 mg/kg, i.p.) inhibits carrageenan-, capsaicin-, and CFA-Induced mechanical and thermal hyperalgesia [5]. Vitexin (10 mg/kg, ip, 30 min before the ipl injection of carrageenan) inhibits pro-inflammatory cytokine (TNF-α, IL-1β, IL-6, and IL-33) and enhances anti-inflammatory cytokine (IL-10) production induced by carrageenan [5].
References:
[1]. He M, Min J W, Kong W L, et al. A review on the pharmacological effects of vitexin and isovitexin[J]. Fitoterapia, 2016, 115: 74-85.
[2]. Choi H J, Eun J S, Kim B G, et al. Vitexin, an HIF-1α Inhibitor, Has Anti-metastatic Potential in PC12 Cells[J]. Molecules & Cells (Springer Science & Business Media BV), 2006, 22(3).
[3]. Yang S H, Liao P H, Pan Y F, et al. The novel p53‐dependent metastatic and apoptotic pathway induced by vitexin in human oral cancer OC2 cells[J]. Phytotherapy Research, 2013, 27(8): 1154-1161.
[4]. Dong L Y, Li S, Zhen Y L, et al. Cardioprotection of vitexin on myocardial ischemia/reperfusion injury in rat via regulating inflammatory cytokines and MAPK pathway[J]. The American Journal of Chinese Medicine, 2013, 41(06): 1251-1266.
[5]. Borghi S M, Carvalho T T, Staurengo-Ferrari L, et al. Vitexin inhibits inflammatory pain in mice by targeting TRPV1, oxidative stress, and cytokines[J]. Journal of Natural Products, 2013, 76(6): 1141-1149.
| Cas No. | 3681-93-4 | SDF | |
| 别名 | 牡荆素,Apigenin 8-C-glucoside; Vitexina; 4H-1-Benzopyran-4-one, 8-β-D-glucopyranosyl-5,7-dihydroxy-2-(4-hydroxyphenyl)- | ||
| 化学名 | 5,7-dihydroxy-2-(4-hydroxyphenyl)-8-[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]chromen-4-one | ||
| Canonical SMILES | C1=CC(=CC=C1C2=CC(=O)C3=C(O2)C(=C(C=C3O)O)C4C(C(C(C(O4)CO)O)O)O)O | ||
| 分子式 | C21H20O10 | 分子量 | 432.38 |
| 溶解度 | DMSO：47 mg/mL (108.7 mM) | 储存条件 | Store at 4°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 | 2.3128 mL | 11.5639 mL | 23.1278 mL |
| 5 mM | 0.4626 mL | 2.3128 mL | 4.6256 mL |
| 10 mM | 0.2313 mL | 1.1564 mL | 2.3128 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。
A review on the pharmacological effects of vitexin and isovitexin
Vitexin and isovitexin are active components of many traditional Chinese medicines, and were found in various medicinal plants. Vitexin (apigenin-8-C-glucoside) has recently received increased attention due to its wide range of pharmacological effects, including but not limited to anti-oxidant, anti-cancer, anti-inflammatory, anti-hyperalgesic, and neuroprotective effects. Isovitexin (apigenin-6-C-glucoside), an isomer of vitexin, generally purified together with vitexin, also exhibits diverse biological activities. Latest research has suggested that vitexin and isovitexin could be potential substitute medicines for diversity diseases, and may be adjuvants for stubborn diseases or health products. This review summarized recent findings on various pharmacological activities and associative signalling pathways of vitexin and isovitexin to provide a reference for future research and clinical applications.
Vitexin inhibits APEX1 to counteract the flow-induced endothelial inflammation
Vascular endothelial cells are exposed to shear stresses with disturbed vs. laminar flow patterns, which lead to proinflammatory vs. antiinflammatory phenotypes, respectively. Effective treatment against endothelial inflammation and the consequent atherogenesis requires the identification of new therapeutic molecules and the development of drugs targeting these molecules. Using Connectivity Map, we have identified vitexin, a natural flavonoid, as a compound that evokes the gene-expression changes caused by pulsatile shear, which mimics laminar flow with a clear direction, vs. oscillatory shear (OS), which mimics disturbed flow without a clear direction. Treatment with vitexin suppressed the endothelial inflammation induced by OS or tumor necrosis factor-α. Administration of vitexin to mice subjected to carotid partial ligation blocked the disturbed flow-induced endothelial inflammation and neointimal formation. In hyperlipidemic mice, treatment with vitexin ameliorated atherosclerosis. Using SuperPred, we predicted that apurinic/apyrimidinic endonuclease1 (APEX1) may directly interact with vitexin, and we experimentally verified their physical interactions. OS induced APEX1 nuclear translocation, which was inhibited by vitexin. OS promoted the binding of acetyltransferase p300 to APEX1, leading to its acetylation and nuclear translocation. Functionally, knocking down APEX1 with siRNA reversed the OS-induced proinflammatory phenotype, suggesting that APEX1 promotes inflammation by orchestrating the NF-κB pathway. Animal experiments with the partial ligation model indicated that overexpression of APEX1 negated the action of vitexin against endothelial inflammation, and that endothelial-specific deletion of APEX1 ameliorated atherogenesis. We thus propose targeting APEX1 with vitexin as a potential therapeutic strategy to alleviate atherosclerosis.
Vitexin reverses the autophagy dysfunction to attenuate MCAO-induced cerebral ischemic stroke via mTOR/Ulk1 pathway
Stroke, as a kind of acute cerebrovascular diseases, has greatly influenced the patients' quality of life and left a huge public health burden. Vitexin is a flavone C-glycoside (apigenin-8-C-?-D-glucopyranoside) present in several medicinal and other plants. This study aims to explore the role of vitexin in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic stroke. The results showed that the MCAO-induced brain infarction was obviously decreased by vitexin. And the abnormal protein levels of Caspase-3, Bcl-2-associated X protein (Bax), antigen identified by monoclonal antibody (Ki-67) and B cell lymphoma 2 (Bcl-2) in MCAO model rats were reversed by vitexin. Further research indicated that vitexin alleviated MCAO-induced oxidative injury by reducing the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA) and nitric Oxide (NO). In addition, vitexin attenuated the secretion of pro-inflammatory cytokine (interleukin (IL)-6 and tumor necrosis factor alpha (TNF-?)) and increased anti-inflammatory cytokine (IL-10) production to ameliorate MCAO-induced inflammation. What's more, vitexin repressed the MCAO-induced autophagy through mechanistic target of rapamycin (mTOR)/Ulk1 pathway. Specifically, the MCAO-induced decreased expression of mTOR, peroxisome proliferator-activated receptor ? (PPAR?) and p62 were inhibited by vitexin. At the same time, MCAO-induced increased expression of Ulk1, Beclin1 and rate of LC3?/LC3? also were repressed by vitexin. But the inhibition of vitexin on the MCAO-induced oxidative injury, apoptosis and inflammation were reversed by rapamycin. These results implied that vitexin suppressed the autophagy dysfunction to attenuate MCAO-induced cerebral ischemic stroke via mTOR/Ulk1 pathway.
Vitexin prevents colitis-associated carcinogenesis in mice through regulating macrophage polarization
Background: Patients with inflammatory bowel disease are at increased risks of developing ulcerative colitis-associated colorectal cancer (CAC). Vitexin can suppress the proliferation of colorectal carcinoma cells in vitro orin vivo. However, different from colorectal carcinoma, CAC is more consistent with the transformation from inflammation to cancer in clinical chronic IBD patients. Therefore, we aim to investigated that vitexin whether possess benefic effects on CAC mice.
Purpose: We aimed to determine the beneficial effects of vitexin on CAC mice and reveal its underlying mechanism.
Methods: The mouse CAC model was induced by Azoxymethane and dextran sodium sulfate (AOM/DSS) and CAC mice were treated with vitexin. At the end of this study, inflammatory cytokines of IL-1β, IL-6, TNF-α, IL-10 as well as nitric oxide (NO) were detected by kits after long-term treatment of vitexin. Pathological changes and macrophage polarization were determined by H&E and immunofluorescence in adjacent noncancerous tissue and carcinomatous tissue respectively of CAC mice.
Results: Our results showed that oral administration of vitexin could significantly improve the clinical signs and symptoms of chronic colitis, relieve colon damage, regulate colonic inflammatory cytokines, as well as suppress tumor incidence and tumor burden. Interesting, vitexin caused a significant increase in serum level of NO and a higher content of NO in tumor tissue. In addition, vitexin significantly decreased M1 phenotype macrophages in the adjacent noncancerous tissue, while markedly up-regulated M1 macrophage polarization in the tumor tissue in the colon of CAC mice.
Conclusion: Vitexin can attenuate chronic colitis-associated carcinogenesis induced by AOM/DSS in mice and its protective effects are partly associated with its alternations in macrophage polarization in the inflammatory and tumor microenvironment .
Vitexin exerts protective effects against calcium oxalate crystal-induced kidney pyroptosis in vivo and in vitro
Background: Nephrolithiasis is a common urinary disease with a high recurrence rate of secondary stone formation. Several mechanisms are involved in the onset and recurrence of nephrolithiasis, e.g., oxidative stress, inflammation, apoptosis, and epithelial-mesenchymal transition (EMT). Vitexin, a flavonoid monomer derived from medicinal plants that exert many biological effects including anti-inflammatory and anticancer effects, has not been investigated in nephrolithiasis studies. Moreover, pyroptosis, a form of programmed cell death resulting from inflammasome-associated caspase activation, has not been studied in mice with nephrolithiasis.
Purpose: We aimed to investigate the protective effect and underlying mechanisms of vitexin in nephrolithiasis, and the related role of pyroptosis in vivo and in vitro.
Methods: Mouse models of nephrolithiasis were established via intraperitoneal injection of glyoxylate, and cell models of tubular epithelial cells and macrophages were established using calcium oxalate monohydrate (COM). Crystal deposition and kidney tissue injury were evaluated by hematoxylin and eosin, and von Kossa staining. Renal oxidative stress indexes including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT), were analyzed. The renal expression of interleukin-1 beta (IL-1β), gasdermin D (GSDMD), osteopontin (OPN), CD44, and monocyte chemotactic protein 1 (MCP-1), and EMT-related proteins in renal tubular epithelial cells was assessed. Cell viability and the apoptosis ratio were evaluated.
Results: In vivo, vitexin alleviated crystal deposition and kidney tissue injury, and decreased the level of MDA, and increased the levels of SOD, GSH, and CAT. Vitexin also reduced the levels of the pyroptosis-related proteins GSDMD, NLRP3, cleaved caspase-1, and mature IL-1β, which were elevated in mice with nephrolithiasis, and repressed apoptosis and the expression of OPN and CD44. Moreover, vitexin mitigated F4/80-positive macrophage infiltration and MCP-1 expression in the kidneys. Furthermore, an in vitro study showed that vitexin increased the viability of HK-2 cells and THP-1-derived macrophages, which was impaired by treatment with COM crystals, decreased the medium lactate dehydrogenase (LDH) level, and inhibited the expression of pyroptosis-related proteins in HK-2 cells and macrophages. Vitexin repressed EMT of HK-2 cells, with increased expression of pan-cytokeratin (Pan-ck) and decreased expression of Vimentin and alpha-smooth muscle actin (α-SMA), and downregulated the Wnt/β-catenin pathway. Moreover, vitexin suppressed tumor necrosis factor-α (TNF-α) and IL-1β mRNA expression, which was upregulated by COM in macrophages.
Conclusion: Vitexin exerts protective effects against nephrolithiasis by inhibiting pyroptosis activation, apoptosis, EMT, and macrophage infiltration. In addition, GSDMD-related pyroptosis mediates nephrolithiasis.