Sappanone A
目录号 : GC41626
Sappanone A is a homoisoflavanone with strong antioxidant and anti-inflammatory activities.
Cas No.:104778-14-5,102067-84-5
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
| Cell experiment [1]: | |
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Cell lines |
Chondrocytes |
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Preparation Method |
Cells were treated with 0, 5, 10, 20, or 40 µM of sappanone A for 24 h. Then, the cells were incubated for 2 h with 10 µl of CCK-8 solution, and the absorbance (450 nm) was detected. |
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Reaction Conditions |
0-40µM；24h |
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Applications |
40 µM sappanone A produced a significant inhibitory effect on cell viability. Concentrations of 5, 10, and 20 µM showed no significant change in cell viability. |
| Animal experiment [2]: | |
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Animal models |
Sprague Dawley rats |
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Preparation Method |
The rats were divided into four groups (eight rats/group) as follows: (A) Normal group, (B) MI group, (C) MI + Curcumin 25 mg/kg group, (D) MI + Sappanone A 50 mg/kg group. The rats in groups A and B received vehicle (10% dimethyl sulfoxide, DMSO, and 90% polyethylene glycol, PEG400), and the rats in groups C and D were treated with 25 mg/kg curcumin, and 50 mg/kg sappanone A dissolved in vehicle by oral injection daily for 5 days. |
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Dosage form |
50 mg/kg；p.o.；5 days |
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Applications |
Sappanone A significantly improved left ventricular (LV) systolic and diastolic function in a rat myocardial ischemia/reperfusion injury model, especially in the early phase development of myocardial infarction. |
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References: [1]. Zhang Z, Zhang NZ, et,al. Sappanone A Alleviated IL-1β-Induced Inflammation in OA Chondrocytes through Modulating the NF-κB and Nrf2/HO-1 Pathways. Dis Markers. 2022 Sep 16;2022:2380879. doi: 10.1155/2022/2380879. PMID: 36157214; PMCID: PMC9507726. |
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Sappanone A is a homoisoflavanone with strong antioxidant and anti-inflammatory activities. It is one of the active ingredients of Sappan Lignum, it can inhibit microglia activation in the brain and has a neuroinflammatory effect[1-2].
Sappanone A(0-30µM；30min) inhibited the production of nitric oxide (NO), prostaglandin E2 (PGE2) and interleukin-6 (IL-6) as well as the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and IL-6 in lipopolysaccharide (LPS)-stimulated RAW264.7 cells[3]. sappanone A (1.1 µM )significantly inhibited IBMX-induced increase of melanin content in B16 cells [4].40 µM sappanone A produced a significant inhibitory effect on cell viability. Concentrations of 5, 10, and 20 µM showed no significant change in cell viability. Sappanone A inhibited the IL-1β-stimulated production of NO, PGE2, iNOS, COX-2, TNF-α, IL-6, and IL-8 in OA chondrocytes[5].Sappanone A decreased cell viability of HOK cells and mouse salivary gland cells under ionising radiation[6].
Sappanone A (12.5, 25 and 50 mg/kg; 3days;i.p.) was found to attenuate the airway inflammation and mucus hypersecretion induced by the Ovalbumin(OVA) challenge in BALB/c mice[7]. Sappanone A(50 mg/kg；p.o.；5 days) significantly improved left ventricular (LV) systolic and diastolic function in a rat myocardial ischemia/reperfusion injury model, especially in the early phase development of myocardial infarction[8]. Sappanone A (10、20、40 mg/kg;i.p. ) reduced myocardial infarct size and the release of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) in a dose-dependent manner in myocardial ischemia reperfusion injury (MIRI) mice [9].
Sappanone A是一种具有较强抗氧化和抗炎活性的同型异黄酮。它是木质素的有效成分之一,可以抑制大脑小胶质细胞的激活,具有神经炎症作用[1-2]。
Sappanone A(0-30µM;30min)可抑制脂多糖(LPS)刺激的RAW264.7细胞中一氧化氮(NO)、前列腺素E2 (PGE2)和白细胞介素6 (IL-6)的生成以及诱导型一氧化氮合酶(iNOS)、环氧合酶-2 (COX-2)和IL-6的表达[3]。sappanone A (1.1 µM)显著抑制IBMX诱导的B16细胞黑色素含量升高[4]。40 µM的sappanone A对细胞活力有明显的抑制作用。5、10、20 µM浓度对细胞活力无显著影响。Sappanone A抑制IL-1β刺激的OA软骨细胞NO、PGE2、iNOS、COX-2、TNF-α、IL-6和IL-8的产生[5]。在电离辐射作用下,Sappanone A可降低HOK细胞和小鼠唾液腺细胞的活力[6]。
Sappanone A(12.5、25和50 mg/kg;3days;i.p.)可减轻BALB/c小鼠因卵清蛋白OVA攻击引起的气道炎症和粘液分泌亢进[7]。在大鼠心肌缺血/再灌注损伤模型中,Sappanone A(50 mg/kg;p.o;5天)显著改善左室(LV)收缩和舒张功能,尤其是在心肌梗死早期发展阶段[8]。Sappanone A(10、20、40 mg/kg; i.p.)以剂量依赖的方式减少了心肌缺血再灌注损伤(MIRI)小鼠的心肌梗死面积和乳酸脱氢酶(LDH)和肌酸激酶-MB(CK-MB)的释放[9]。
References:
[1]. Kang L, Zhao H, et,al. Sappanone A protects mice against cisplatin-induced kidney injury. Int Immunopharmacol. 2016 Sep;38:246-51. doi: 10.1016/j.intimp.2016.05.019. Epub 2016 Jun 16. PMID: 27318179.
[2]. Syamsunarno MRA, Safitri R, et,al.Protective Effects of Caesalpinia sappan Linn. and Its Bioactive Compounds on Cardiovascular Organs. Front Pharmacol. 2021 Sep 15;12:725745. doi: 10.3389/fphar.2021.725745. PMID: 34603037; PMCID: PMC8479160.
[3]. Lee S, Choi SY, et,al.Sappanone A exhibits anti-inflammatory effects via modulation of Nrf2 and NF-κB. Int Immunopharmacol. 2015 Sep;28(1):328-36. doi: 10.1016/j.intimp.2015.06.015. Epub 2015 Jun 26. PMID: 26122134.
[4]. Chang TS, Chao SY, et,al.Melanogenesis inhibition by homoisoflavavone sappanone A from Caesalpinia sappan. Int J Mol Sci. 2012;13(8):10359-10367. doi: 10.3390/ijms130810359. Epub 2012 Aug 20. PMID: 22949866; PMCID: PMC3431864.
[5]. Zhang Z, Zhang NZ, et,al. Sappanone A Alleviated IL-1β-Induced Inflammation in OA Chondrocytes through Modulating the NF-κB and Nrf2/HO-1 Pathways. Dis Markers. 2022 Sep 16;2022:2380879. doi: 10.1155/2022/2380879. PMID: 36157214; PMCID: PMC9507726.
[6]. Zhao XF, Wang ZY, et,al.Sappanone A Aggrandises Ionising Radiation-induced Damage in Oral Epithelial Cells. Chin J Dent Res. 2022 Dec 8;25(4):261-267. doi: 10.3290/j.cjdr.b3628117. PMID: 36479890.
[7]. Liu X, Yu D, et,al.Sappanone A Attenuates Allergic Airway Inflammation in Ovalbumin-Induced Asthma. Int Arch Allergy Immunol. 2016;170(3):180-6. doi: 10.1159/000448331. Epub 2016 Aug 30. PMID: 27576536.
[8]. Jo W, Min BS, et,al.Sappanone A Prevents Left Ventricular Dysfunction in a Rat Myocardial Ischemia Reperfusion Injury Model. Int J Mol Sci. 2020 Sep 21;21(18):6935. doi: 10.3390/ijms21186935. PMID: 32967328; PMCID: PMC7555706.
[9].Shi X, Tao G, et,al. Sappanone A Protects Against Myocardial Ischemia Reperfusion Injury by Modulation of Nrf2. Drug Des Devel Ther. 2020 Jan 8;14:61-71. doi: 10.2147/DDDT.S230358. PMID: 32021092; PMCID: PMC6955610.
| Cas No. | 104778-14-5,102067-84-5 | SDF | |
| Canonical SMILES | OC1=CC=C(C(/C(CO2)=C/C3=CC=C(O)C(O)=C3)=O)C2=C1 | ||
| 分子式 | C16H12O5 | 分子量 | 284.3 |
| 溶解度 | DMF: 20 mg/ml,DMSO: 15 mg/ml,Ethanol: 5 mg/ml,PBS (pH 7.2): 0.25 mg/ml | 储存条件 | Store at -20°C,protect from light |
| 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 | 3.5174 mL | 17.5871 mL | 35.1741 mL |
| 5 mM | 0.7035 mL | 3.5174 mL | 7.0348 mL |
| 10 mM | 0.3517 mL | 1.7587 mL | 3.5174 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。
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Sappanone A Aggrandises Ionising Radiation-induced Damage in Oral Epithelial Cells
Chin J Dent Res 2022 Dec 8;25(4):261-267.PMID:36479890DOI:10.3290/j.cjdr.b3628117.
Objective: To analyse the role played by Sappanone A, a bioactive ingredient isolated from the heartwood of Caesalpinia sappan, in the regulation of oral epithelial cell viability under radiation. Methods: Cell viability of human oral keratinocytes (HOKs) and mouse salivary gland cells under ionising radiation was analysed. Expression of Ki67 was measured by immunohistochemical staining. Fragmentation of deoxyribonucleic acid (DNA) was measured by comet assay. Cell death was analysed using trypan blue exclusion assay. Cell viability was measured using a Cell Counting Kit 8 (CCK8; Abcam, Cambridge, UK) assay. Results: Sappanone A decreased cell viability of HOK cells and mouse salivary gland cells under ionising radiation. In addition, Sappanone A enhanced radiation-induced genomic DNA fragmentation, accompanied by impaired homologous recombination and non-homologous end joining DNA repair. Mechanistic evaluation revealed that Sappanone A counteracted radiation-induced inosine monophosphate dehydrogenase 2 (IMPDH2) activation, and that this effect could be abolished by reconstituted expression of a Sappanone A-binding defective IMPDH2 mutant. Conclusion: The present study highlights a novel role played by Sappanone A in the modulation of radiosensitivity of oral epithelial cells.
Sappanone A ameliorates acetaminophen-induced acute liver injury in mice
Toxicology 2022 Oct;480:153336.PMID:36126895DOI:10.1016/j.tox.2022.153336.
Sappanone A (SA), a homoisoflavonoid compound extracted from the heartwood of Caesalpinia sappan Linn., exerts anti-inflammatory and antioxidant activities. However, the effects of SA on acetaminophen (APAP) overdose-induced acute liver injury (ALI) have not been determined yet. This study aims to explore the protective effects of SA and the potential mechanisms of action. Mice were pretreated with SA (25, 50, and 100 mg/kg) by intraperitoneal (i.p.) injection for seven days prior to APAP (300 mg/kg, i.p.) administration. At 12 h after APAP injection, serum and liver samples were collected. Primary murine hepatocytes were used to investigate the underlying mechanisms. SA pretreatment dose-dependently attenuated APAP-induced ALI, as validated by reduced serum alanine/aspartate aminotransferase levels, histopathologic lesions, and oxidative stress. Consistently, pretreatment with SA reduced the formation of APAP protein adducts in damaged livers of mice. Mechanistically, SA could facilitate the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and thus promote cellular glutathione (GSH) synthesis. The hepatoprotective outcomes provided by SA were significantly abolished by treatment with ML385, a Nrf2 inhibitor. Besides, anti-inflammatory property of SA reduced inflammatory reaction in injured livers of mice. Of note, posttreatment with SA reveals significant therapeutic influences against APAP-induced ALI in mice. Collectively, our findings demonstrated that pretreated-SA ameliorated APAP-mediated ALI in mice, at least in part, by reducing the generation of APAP protein adducts via Nrf2-enhanced GSH synthesis, and by diminishing hepatic inflammation. Therefore, SA could be a potential hepatoprotective agent for treating ALI.
Sappanone A Alleviated IL-1 β-Induced Inflammation in OA Chondrocytes through Modulating the NF- κ B and Nrf2/HO-1 Pathways
Dis Markers 2022 Sep 16;2022:2380879.PMID:36157214DOI:10.1155/2022/2380879.
Objective: This study was to examine the anti-inflammatory effect of Sappanone A on interleukin- (IL-) 1β-stimulated osteoarthritis (OA) chondrocytes. Methods: Chondrocytes were pretreated with Sappanone A for 2 h before subsequent IL-1β stimulation. The mRNA expression levels of iNOs, COX-2, aggrecan, and collagen-II were measured with qRT-PCR. The levels of TNF-α, IL-6, IL-8, MMP-3, and MMP-13 were determined by ELISA. The protein levels of iNOs, COX-2, ADAMTS-4, ADAMTS-5, aggrecan, collagen-II, p-p65, p65, IκBα, Nrf2, and HO-1 were assessed by Western blot. Results: Sappanone A inhibited the IL-1β-stimulated production of NO, PGE2, iNOS, COX-2, TNF-α, IL-6, and IL-8 in OA chondrocytes. In addition, Sappanone A suppressed the expression of MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 in IL-1β-stimulated OA chondrocytes. The degradation of ECM components was reversed by Sappanone A. Sappanone A prevented NF-κB activation while enhanced Nrf2/HO-1 activation in IL-1β-treated chondrocytes. Conclusion: Sappanone A may be a potent therapeutic agent for OA.
Sappanone A Prevents Left Ventricular Dysfunction in a Rat Myocardial Ischemia Reperfusion Injury Model
Int J Mol Sci 2020 Sep 21;21(18):6935.PMID:32967328DOI:10.3390/ijms21186935.
The incidence of myocardial infarction, among the causes of cardiovascular morbidity and mortality, is increasing globally. In this study, left ventricular (LV) dysfunction, including LV systolic and diastolic function, was investigated in a rat myocardial ischemia/reperfusion injury model with echocardiography. The homoisoflavanone Sappanone A is known for its anti-inflammatory effects. Using echocardiography, we found that Sappanone A administration significantly improved LV systolic and diastolic function in a rat myocardial ischemia/reperfusion injury model, especially in the early phase development of myocardial infarction. Based on myocardial infarct size, serum cardiac marker assay, and histopathological evaluation, Sappanone A showed higher efficacy at the doses used in our experiments than curcumin and was evaluated for its potential to improve LV function.
Sappanone A Protects Against Myocardial Ischemia Reperfusion Injury by Modulation of Nrf2
Drug Des Devel Ther 2020 Jan 8;14:61-71.PMID:32021092DOI:10.2147/DDDT.S230358.
Background: Oxidative stress is a major contributor to the onset and development of myocardial ischemia reperfusion injury (MIRI). Sappanone A (SA), a homoisoflavanone extracted from the heartwood of Caesalpinia sappan L., has been demonstrated to possess powerful antioxidant activity. Therefore, this study aimed to determine the protective effect of SA on MIRI and investigate its underlying mechanism. Methods: The rat hearts were isolated and underwent 30-min ischemia, followed by 120-min reperfusion to establish the MIRI model, using the Langendorff method. SA was administrated intraperitoneally into rats 1 h prior to heart isolation. The myocardial infarct size and apoptosis were measured by TTC and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Myocardial enzyme activity, MDA content and the activities of SOD and GSH-Px were detected by colorimetric spectrophotometric method. Reactive oxygen species (ROS) level was detected by DCFH-DA probe. The change in Keap1/Nrf2 signaling pathway was evaluated by Western blotting. Results: SA reduced myocardial infarct size and the release of CK-MB and LDH in a dose-dependent manner. Moreover, SA improved the recovery of cardiac function, inhibited MIRI-induced apoptosis, repressed the production of ROS and MDA, and enhanced the activities of SOD and GSH-Px. Mechanistically, SA downregulated Keap1, induced Nrf2 nuclear accumulation, and enhanced Nrf2 transcriptional activity, subsequently resulting in an increase in the expression of the Nrf2 target genes heme oxygenase-1 and NAD(P)H quinone dehydrogenase 1. Moreover, SA enhanced the phosphorylation of Nfr2, but the enhancement in Nfr2 phosphorylation was abrogated by PKC or PI3K inhibitor. Conclusion: Collectively, it was demonstrated that SA prevents MIRI via coordinating the cellular antioxidant defenses and maintaining the redox balance, by modulation of Nrf2 via the PKC or PI3K pathway. Therefore, SA was a potential therapeutic drug for treating MIRI.