Butin
(Synonyms: 紫铆亭) 目录号 : GC61409
Butin是从黄檀的心材中分离出的主要的一种生物活性黄酮类化合物，具有很强的抗氧化、抗血小板和抗炎活性。在大鼠中，Butin能显著减轻心肌梗死现象，改善心脏功能，预防糖尿病引起的心脏氧化损伤。
Cas No.:21913-99-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Butin is a major biologically active flavonoid isolated from the heartwood of Dalbergia odorifera, with strong antioxidant, antiplatelet and anti-inflammatory activities. Butin significantly alleviates myocardial infarction and improves heart function, together with prevents diabetes-induced cardiac oxidative damage in rat[1][2].
[1]. Duan J, et al. Protective effect of butin against ischemia/reperfusion-induced myocardial injury in diabetic mice: involvement of the AMPK/GSK-3β/Nrf2 signaling pathway. Sci Rep. 2017 Jan 27;7:41491. [2]. Li P, et al. Butin Attenuates Brain Edema in a Rat Model of Intracerebral Hemorrhage by Anti Inflammatory Pathway. Transl Neurosci. 2018 May 8;9:7-12.
| Cas No. | 21913-99-5 | SDF | |
| 别名 | 紫铆亭 | ||
| Canonical SMILES | O=C1CC(C2=CC=C(O)C(O)=C2)OC3=CC(O)=CC=C13 | ||
| 分子式 | C15H12O5 | 分子量 | 272.25 |
| 溶解度 | DMSO: 41.67 mg/mL (153.06 mM) | 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 | 3.6731 mL | 18.3655 mL | 36.7309 mL |
| 5 mM | 0.7346 mL | 3.6731 mL | 7.3462 mL |
| 10 mM | 0.3673 mL | 1.8365 mL | 3.6731 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。
Butin Mitigates Memory Impairment in Streptozotocin-Induced Diabetic Rats by Inhibiting Oxidative Stress and Inflammatory Responses
Metabolites 2022 Nov 1;12(11):1050.PMID:36355133DOI:10.3390/metabo12111050.
It has been reported from the previous literature that Butin restores mitochondrial dysfunction by modulation of oxidative stress and glutamate-induced neurotoxicity in mouse hippocampus HT22 cells. Butin also possesses an anti-Huntington's effect in rats. Considering the current background, this study was designed to evaluate the neuroprotective effect of Butin against memory loss caused by streptozotocin (STZ). STZ (40 mg/kg) was intraperitoneally injected into rats. Three days later, diabetic rats were identified and included in the study. A total of 30 rats (12 nondiabetic and 18 diabetics) were grouped as Group A (control-non-diabetic rats) and Group B (STZ diabetic control) were treated with 1 mL of sodium CMC (0.5% w/v). Group C (STZ+ Butin 25) were treated with Butin 25 mg/kg. Group D (STZ+ Butin 50) and Group E (Butin per se) were administered with Butin 50 mg/kg. Each therapy was administered orally once each day for 15-day. The Morris water maze and the Y-maze behavioural tests were run throughout the experimental programme. Animals were put to death on day 15 and their brains were removed for biochemical assays (CAT, SOD, GSH, MDA, nitrite, acetylcholinesterase (AchE), IL-1, and mitochondrial enzyme complexes). Rats with neurobehavioral impairments brought on by STZ have less spontaneous movement, learning capacity, and memory. Additionally, STZ decreased endogenous antioxidants and increased pro-inflammatory cytokines, nitrite, MDA, and AchE. Neurobehavioral deficits and metabolic markers were dramatically improved by Butin.
Anti-Huntington's Effect of Butin in 3-Nitropropionic Acid-Treated Rats: Possible Mechanism of Action
Neurotox Res 2022 Feb;40(1):66-77.PMID:34982357DOI:10.1007/s12640-021-00462-7.
Butin has a strong antioxidant plus anti-inflammatory action and it is reported to be protective in oxidative stress-induced mitochondrial dysfunction. Butin has been shown to protect the mouse hippocampus HT22 cells from glutamate-induced neurotoxicity. The current investigation was planned to assess anti-Huntington's effect of Butin in 3-nitropropionic acid-treated rats. A total of 32 Wistar rats (200-240 g) were equally segregated into four groups. Groups I and II were treated with vehicle (0.3 ml/100 g) and groups III and IV received Butin 25 and 50 mg/kg for 15 days. Daily 1 h post above oral treatments, 3 ml/kg of normal saline was injected (i.p.) to group I animals and 10 mg/kg of 3-NP was injected (i.p.) to II and IV groups for 15 days. During the experimental schedule, behavioral tests were conducted for animals. On day 15, after behavioral parameters, animals were sacrificed and brains were removed for biochemical tests. Systemic administration of 3-NP induced neurobehavioral deficits which resulted in reduced spontaneous locomotor activity, motor incoordination, learning ability, and memory in the animals. Moreover, 3-NP depleted endogenous antioxidants (GSH, catalase, and SOD), mitochondrial complexes activities (I, II, IV, and MTT assay), elevated LDH, MDA, nitrite, and AchE. Administration of Butin significantly improved neurobehavioral impairments, nitrative and oxidative stress, activities of mitochondrial enzyme complex, and reduced AchE levels in rat brain.
Butin Attenuates Arthritis in Complete Freund's Adjuvant-Treated Arthritic Rats: Possibly Mediated by Its Antioxidant and Anti-Inflammatory Actions
Front Pharmacol 2022 Feb 15;13:810052.PMID:35242033DOI:10.3389/fphar.2022.810052.
The present research work was planned to evaluate the antioxidant and anti-inflammatory actions of Butin in preventing complete Freund's adjuvant-induced arthritis in rats. Adult Wistar rats (200-240 g) were segregated equally into four groups: Group I (normal) and Group II complete Freund's adjuvant (CFA control) were administered orally with 3 ml/kg of 0.5% SCMC (vehicle); Group III and Group IV were test groups and orally administered 25 and 50 mg/kg of Butin. These oral treatments were administered for a total of 21 days. In the 21-day treatment schedule, on the first day, animals from group I (normal control) were injected a single dose of normal saline (0.1 ml) intradermally into one of the hind paws, and animals from Group II to IV were injected CFA (0.1 ml) intradermally into one of the hind paws. During the treatment schedule, the volume of the hind paw and body weight were recorded at every 7 days intervals, and animals were scored for severe arthritis on days 17, 19, and 21. On the 22nd day, samples of blood were withdrawn by puncturing the retro-orbital sinus for analysis of RBC, WBC, hemoglobin, ALT, AST, ALP, PGE2, and cytokines. After blood withdrawal, animals were euthanized; the paw was separated by cutting at the ankle joint and used for analysis of oxidative stress and antioxidant parameters, as well as for the histopathological study. Administration of Butin to CFA-treated animals significantly attenuated the CFA-induced inflammatory response, oxidative stress, and reversed the histopathological alteration towards normal. According to the findings, Butin has anti-inflammatory and anti-arthritic properties in rats with CFA-induced arthritis.
Butin Attenuates Brain Edema in a Rat Model of Intracerebral Hemorrhage by Anti Inflammatory Pathway
Transl Neurosci 2018 May 8;9:7-12.PMID:29755784DOI:10.1515/tnsci-2018-0002.
Background: This study evaluates the effect of Butin against brain edema in intracerebral hemorrhage (ICH). Methodology: ICH was induced by injecting bacterial collagenase in the brain and all the animals were separated into four groups such as control group, ICH group treated with vehicle, Butin 25 and 50 mg/kg group receives Butin (25 and 50 mg/kg, i.p.)60 min after the induction of ICH in all animals. One day after neurological score, hemorrhagic injury and expressions of protein responsible for apoptosis and inflammatory cytokines were assessed in the brain tissue of ICH rats. Result: Neurological scoring significantly increased and hemorrhagic lesion volume decreased in Butin treated group of rats compared to ICH group. However, treatment with Butin significantly decreases the ratio of Bax/Bcl-2 and protein expression of Cleaved caspase-3 than ICH group in dose dependent manner. Level of inflammatory mediators such as tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6) in the brain tissues were significantly decreased in the Butin treated group than ICH group. In addition Butin attenuates the altered signaling pathway of NF-κB in the brain tissues of ICH rats. Conclusion: Our study concludes that Butin attenuates the altered behavior and neuronal condition in ICH rats by reducing apoptosis and inflammatory response.
Butin reduces oxidative stress-induced mitochondrial dysfunction via scavenging of reactive oxygen species
Food Chem Toxicol 2010 Mar;48(3):922-7.PMID:20060874DOI:10.1016/j.fct.2010.01.001.
This study investigated the cytoprotective effect of Butin, a flavonoid, on hydrogen peroxide (H(2)O(2))-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed Butin's significant scavenging effects on superoxide radicals and hydroxyl radicals. When H(2)O(2) was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster lung fibroblast (V79-4) cells, Butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca(2+) levels that have been induced by H(2)O(2). Furthermore, Butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H(2)O(2) treatment. We conclude these results suggest Butin decreased mitochondrial ROS accumulation, balanced intracellular Ca(2+) levels, and improved mitochondrial energy production, thus recovering mitochondrial function.