Lithospermic acid
(Synonyms: 紫草酸; (+)-Lithospermic acid) 目录号 : GC38187
A polyphenol with diverse biological activities
Cas No.:28831-65-4
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
Lithospermic acid is a polyphenol that has been found in S. miltiorrhiza and has diverse biological activities.1,2 It inhibits xanthine oxidase (IC50 = 5.2 ?g/ml) and scavenges DPPH radicals in cell-free assays (IC50 = 23.2 ?g/ml). It also inhibits the production of reactive oxygen species (ROS) induced by phorbol 12-myristate 13-acetate in isolated human neutrophils in a concentration-dependent manner.1 Lithospermic acid inhibits 3'-processing and 3'-joining to target DNA by HIV-1 integrase in cell-free assays (IC50s = 0.83 and 0.48 ?M, respectively).3 It also inhibits acute HIV-1 infection of H9 human lymphoma cells (IC50 = 2 ?M) without inducing cytotoxicity. Lithospermic acid (100 mg/kg) prevents carbon tetrachloride-induced hepatic necrosis in mice.2
1.Liu, X., Chen, R., Shang, Y., et al.Lithospermic acid as a novel xanthine oxidase inhibitor has anti-inflammatory and hypouricemic effects in ratsChem. Biol. Interact.176(2-3)137-142(2008) 2.Chan, K.W.K., and Ho, W.S.Anti-oxidative and hepatoprotective effects of lithospermic acid against carbon tetrachloride-induced liver oxidative damage in vitro and in vivoOncol. Rep.34(2)673-680(2015) 3.Abd-Elazem, I.S., Chen, H.S., Bates, R.B., et al.Isolation of two highly potent and non-toxic inhibitors of human immunodeficiency virus type 1 (HIV-1) integrase from Salvia miltiorrhizaAntiviral Res.55(1)91-106(2002)
| Cas No. | 28831-65-4 | SDF | |
| 别名 | 紫草酸; (+)-Lithospermic acid | ||
| Canonical SMILES | O=C([C@@H]1[C@@H](C2=CC=C(O)C(O)=C2)OC3=C(O)C=CC(/C=C/C(O[C@@H](C(O)=O)CC4=CC=C(O)C(O)=C4)=O)=C13)O | ||
| 分子式 | C27H22O12 | 分子量 | 538.46 |
| 溶解度 | Soluble in DMSO | 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 | 1.8571 mL | 9.2857 mL | 18.5715 mL |
| 5 mM | 0.3714 mL | 1.8571 mL | 3.7143 mL |
| 10 mM | 0.1857 mL | 0.9286 mL | 1.8571 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。
Diastereomers of Lithospermic acid and Lithospermic acid B from Monarda fistulosa and Lithospermum erythrorhizon
Fitoterapia 2013 Dec;91:51-59.PMID:23978578DOI:10.1016/j.fitote.2013.08.009.
Monardic acids A (1) and B (2), which are (7R,8R) diastereomers of Lithospermic acid (LA) and Lithospermic acid B, respectively, were isolated from Monarda fistulosa. A (7S,8R) isomer (3) of LA was also isolated from this plant, and a (7R,8S) isomer (7) of LA was obtained from Lithospermum erythrorhizon. The absolute configuration of 1 was confirmed by analysis of its hydrolysates, 7-epiblechnic acid and 2R-3-(3,4-dihydroxyphenyl)-2-hydroxypropanoic acid. The configuration in the dihydrobenzofuran moieties of 2, 3, and 7 was extrapolated by using the phenylglycine methyl ester method and a Cotton effect at approximately 250-260 nm in their electronic circular dichroism spectra. Diastereomers (1-3 and 7) displayed moderate hyaluronidase inhibitory and histamine release inhibitory activities.
Inhibitory Effect of Lithospermic acid on the HIV-1 Nucleocapsid Protein
Molecules 2020 Nov 20;25(22):5434.PMID:33233563DOI:10.3390/molecules25225434.
The HIV-1 nucleocapsid protein (NC) is a desirable target in antiretroviral therapy due to its high conservation among HIV-1 strains, and to its multiple and crucial roles in the HIV-1 replication cycle. Natural products represent a valuable source of NC inhibitors, with the catechol group being a privileged scaffold in NC inhibition. By coupling molecular modeling with NMR spectroscopy and fluorescence-based assays, we disclosed Lithospermic acid, a catechol derivative extracted from Salvia miltiorrhizza, as a potent and chemically stable non-covalent inhibitor of the NC. Being different from other catechol derivative reported so far, Lithospermic acid does not undergo spontaneous oxidation in physiological conditions, thus becoming a profitable starting point for the development of efficient NC inhibitors.
Lithospermic acid attenuates 1-methyl-4-phenylpyridine-induced neurotoxicity by blocking neuronal apoptotic and neuroinflammatory pathways
J Biomed Sci 2015 May 28;22(1):37.PMID:26018660DOI:10.1186/s12929-015-0146-y.
Background: Parkinson's disease is the second most common neurodegenerative disorders after Alzheimer's disease. The main cause of the disease is the massive degeneration of dopaminergic neurons in the substantia nigra. Neuronal apoptosis and neuroinflammation are thought to be the key contributors to the neuronal degeneration. Results: Both CATH.a cells and ICR mice were treated with 1-methyl-4-phenylpyridin (MPP(+)) to induce neurotoxicity in vitro and in vivo. Western blotting and immunohistochemistry were also used to analyse neurotoxicity, neuroinflammation and aberrant neurogenesis in vivo. The experiment in CATH.a cells showed that the treatment of MPP(+) impaired intake of cell membrane and activated caspase system, suggesting that the neurotoxic mechanisms of MPP(+) might include both necrosis and apoptosis. Pretreatment of Lithospermic acid might prevent these toxicities. Lithospermic acid possesses specific inhibitory effect on caspase 3. In mitochondria, MPP(+) caused mitochondrial depolarization and induced endoplasmic reticulum stress via increasing expression of chaperone protein, GRP-78. All the effects mentioned above were reduced by Lithospermic acid. In animal model, the immunohistochemistry of mice brain sections revealed that MPP(+) decreased the amount of dopaminergic neurons, enhanced microglia activation, promoted astrogliosis in both substantia nigra and hippocampus, and MPP(+) provoked the aberrant neurogenesis in hippocampus. Lithospermic acid significantly attenuates all of these effects induced by MPP(+). Conclusions: Lithospermic acid is a potential candidate drug for the novel therapeutic intervention on Parkinson's disease.
Lithospermic acid and ischemia/reperfusion injury of the rat small intestine prevention
Adv Clin Exp Med 2012 Jul-Aug;21(4):433-9.PMID:23240448doi
Background: Intestinal ischemia and reperfusion (I-R) injury of different causes, including cardiac insufficiency, sepsis, vasodepressant and cardiodepressant drugs, and complications of long-lasting surgery, represents a major clinical problem. Objectives: The purpose of the present study was to investigate whether Lithospermic acid (LA) can reduce oxidative stress and histological damage in the rat small bowel subjected to mesenteric I-R injury. Material and methods: The study was performed on three groups of animals, each composed of 7 rats: the SO (sham operation) group, the I-R/Untreated group and the I-R/LA (I-R plus LA pretreatment) group. Intestinal ischemia for 45 minutes and reperfusion for 60 minutes were applied. Ileum specimens were obtained to determine the tissue level of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and myeloperoxidase (MPO) activities and histological changes. Results: Untreated intestinal I-R resulted in increased tissue MDA and MPO levels and diminished SOD and GPx activities. These changes were found to be almost reversed in the LA treatment group. Histopathologically, the intestinal injury in rats treated with LA was less than the untreated I-R group. Conclusions: Lithospermic acid attenuates mesenteric ischemia reperfusion injury in rat intestines by increasing tissue SOD and GPx activities and decreasing MDA and MPO levels. Lithospermic acid also improves morphological alterations which occurred after periods of reperfusion.
Activation of Nrf2 by Lithospermic acid Ameliorates Myocardial Ischemia and Reperfusion Injury by Promoting Phosphorylation of AMP-Activated Protein Kinase α (AMPK α)
Front Pharmacol 2021 Nov 26;12:794982.PMID:34899356DOI:10.3389/fphar.2021.794982.
Background: As a plant-derived polycyclic phenolic carboxylic acid isolated from Salvia miltiorrhiza, Lithospermic acid (LA) has been identified as the pharmacological management for neuroprotection and hepatoprotection. However, the role and mechanism of Lithospermic acid in the pathological process of myocardial ischemia-reperfusion injury are not fully revealed. Methods: C57BL/6 mice were subjected to myocardial ischemia and reperfusion (MI/R) surgery and pretreated by LA (50 mg/kg, oral gavage) for six consecutive days before operation. The in vitro model of hypoxia reoxygenation (HR) was induced by hypoxia for 24 h and reoxygenation for 6 h in H9C2 cells, which were subsequently administrated with Lithospermic acid (100 μM). Nrf2 siRNA and dorsomorphin (DM), an inhibitor of AMPKα, were used to explore the function of AMPKα/Nrf2 in LA-mediated effects. Results: LA pretreatment attenuates infarct area and decreases levels of TnT and CK-MB in plasm following MI/R surgery in mice. Echocardiography and hemodynamics indicate that LA suppresses MI/R-induced cardiac dysfunction. Moreover, LA ameliorates oxidative stress and cardiomyocytes apoptosis following MI/R operation or HR in vivo and in vitro. In terms of mechanism, LA selectively activates eNOS, simultaneously increases nuclear translocation and phosphorylation of Nrf2 and promotes Nrf2/HO-1 pathway in vivo and in vitro, while cardioprotection of LA is abolished by pharmacological inhibitor of AMPK or Nrf2 siRNA in H9C2 cells. Conclusion: LA protects against MI/R-induced cardiac injury by promoting eNOS and Nrf2/HO-1 signaling via phosphorylation of AMPKα.