Boldine
(Synonyms: 波尔定) 目录号 : GC40876
An alkaloid with diverse biological activities
Cas No.:476-70-0
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
Boldine is an aporphine isoquinoline alkaloid extracted from the root of Litsea cubeba and also possesses these properties, including antioxidant, anti-inflammatory and cytoprotective effects. Boldine suppresses osteoclastogenesis, improves bone destruction by down-regulating the OPG/RANKL/RANK signal pathway and may be a potential therapeutic agent for rheumatoid arthritis[1].
References:
[1]. Zhao H , et al. Boldine isolated from Litsea cubeba inhibits bone resorption by suppressing the osteoclast differentiation in collagen-induced arthritis. Int Immunopharmacol. 2017 Oct;51:114-123.
| Cas No. | 476-70-0 | SDF | |
| 别名 | 波尔定 | ||
| Canonical SMILES | OC1=C(OC)C2=C3[C@](N(C)CCC3=C1)([H])CC4=CC(O)=C(OC)C=C42 | ||
| 分子式 | C19H21NO4 | 分子量 | 327.4 |
| 溶解度 | DMF: 50 mg/mL,DMSO: 50 mg/mL,DMSO:PBS (pH 7.2) (1:1): 0.5 mg/mL,Ethanol: 30 mg/mL | 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 | 3.0544 mL | 15.2718 mL | 30.5437 mL |
| 5 mM | 0.6109 mL | 3.0544 mL | 6.1087 mL |
| 10 mM | 0.3054 mL | 1.5272 mL | 3.0544 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。
Boldine Ameliorates Vascular Oxidative Stress and Endothelial Dysfunction: Therapeutic Implication for Hypertension and Diabetes
J Cardiovasc Pharmacol 2015 Jun;65(6):522-31.PMID:25469805DOI:10.1097/FJC.0000000000000185.
Epidemiological and clinical studies have demonstrated that a growing list of natural products, as components of the daily diet or phytomedical preparations, are a rich source of antioxidants. Boldine [(S)-2,9-dihydroxy-1,10-dimethoxy-aporphine], an aporphine alkaloid, is a potent antioxidant found in the leaves and bark of the Chilean boldo tree. Boldine has been extensively reported as a potent "natural" antioxidant and possesses several health-promoting properties like anti-inflammatory, antitumor promoting, antidiabetic, and cytoprotective. Boldine exhibited significant endothelial protective effect in animal models of hypertension and diabetes mellitus. In isolated thoracic aorta of spontaneously hypertensive rats, streptozotocin-induced diabetic rats, and db/db mice, repeated treatment of Boldine significantly improved the attenuated acetylcholine-induced endothelium-dependent relaxations. The endothelial protective role of Boldine correlated with increased nitric oxide levels and reduction of vascular reactive oxygen species via inhibition of the nicotinamide adenine dinucleotide phosphate oxidase subunits, p47 and nicotinamide adenine dinucleotide phosphate oxidase 2, and angiotensin II-induced bone morphogenetic protein-4 oxidative stress cascade with downregulation of angiotensin II type 1 receptor and bone morphogenetic protein-4 expression. Taken together, it seems that Boldine may exert protective effects on the endothelium via several mechanisms, including protecting nitric oxide from degradation by reactive oxygen species as in oxidative stress-related diseases. The present review supports a complimentary therapeutic role of the phytochemical, Boldine, against endothelial dysfunctions associated with hypertension and diabetes mellitus by interfering with the oxidative stress-mediated signaling pathway.
Boldine and its antioxidant or health-promoting properties
Chem Biol Interact 2006 Jan 5;159(1):1-17.PMID:16221469DOI:10.1016/j.cbi.2005.09.002.
The increasing recognition of the participation of free radical-mediated oxidative events in the initiation and/or progression of cardiovascular, tumoural, inflammatory and neurodegenerative disorders, has given rise to the search for new antioxidant molecules. An important source of such molecules has been plants for which there is an ethno-cultural base for health promotion. An important example of this is boldo (Peumus boldus Mol.), a chilean tree whose leaves have been traditionally employed in folk medicine and is now widely recognized as a herbal remedy by a number of pharmacopoeias. Boldo leaves are rich in several aporphine-like alkaloids, of which Boldine is the most abundant one. Research conducted during the early 1990s led to the discovery that Boldine is one of the most potent natural antioxidants. Prompted by the latter, a large and increasing number of studies emerged, which have focused on characterizing some of the pharmacological properties that may arise from the free radical-scavenging properties of Boldine. The present review attempts to exhaustively cover and discuss such studies, placing particular attention on research conducted during the last decade. Mechanistic aspects and structure-activity data are discussed. The review encompasses pharmacological actions, which arise from its antioxidant properties (e.g., cyto-protective, anti-tumour promoting, anti-inflammatory, anti-diabetic and anti-atherogenic actions), as well as those that do not seem to be associated with such activity (e.g., vasorelaxing, anti-trypanocidal, immuno- and neuro-modulator, cholagogic and/or choleretic actions). Based on the pharmacological and toxicological data now available, further research needs and recommendations are suggested to define the actual potential of Boldine for its use in humans.
Boldine, an Alkaloid from Peumus boldus Molina, Induces Endothelium-Dependent Vasodilation in the Perfused Rat Kidney: Involvement of Nitric Oxide and Small-Conductance Ca2+-Activated K+ Channel
Evid Based Complement Alternat Med 2022 Feb 16;2022:4560607.PMID:35222671DOI:10.1155/2022/4560607.
Boldine, 2,9-dihydroxy-1,10-dimethoxyaporphine, is the main alkaloid found in the leaves and bark of Peumus boldus Molina. In recent years, Boldine has demonstrated several pharmacological properties that benefit endothelial function, blood pressure control, and reduce damage in kidney diseases. However, the renal vasodilator effects and mechanisms remain unknown. Herein, perfused rat kidneys were used to study the ability of Boldine to induce vasodilation of renal arteries. For that, left kidney preparations with and without functional endothelium were contracted with phenylephrine and received 10-300 nmol Boldine injections. The preparations were then perfused for 15 min with phenylephrine plus L-NAME, indomethacin, KCl, tetraethylammonium, glibenclamide, apamin, charybdotoxin, or iberiotoxin. In 30, 100, and 300 nmol doses, Boldine induced a dose-and endothelium-dependent relaxing effect on the renal vascular bed. No vasodilator effects were observed in preparations lacking functional endothelium. While the inhibition of the cyclooxygenase enzyme through the addition of indomethacin did not cause any change in the vasodilating action of Boldine, the nonselective nitric oxide synthase inhibitor L-NAME fully precluded the vasodilatory action of Boldine at all doses tested. The perfusion with KCl or tetraethylammonium (nonselective K+ channels blocker) also abolished the vasodilatory effect of Boldine, indicating the participation of K+ channels in the renal action of Boldine. The perfusion with glibenclamide (selective ATP-sensitive K+ channels blocker), iberiotoxin (selective high-conductance Ca2+-activated K+ channel blocker), and charybdotoxin (selective high- and intermediate-conductance Ca2+-activated K+ channel blocker) did not modify the vasodilatory action of Boldine. On the other hand, the perfusion with apamin (selective small-conductance Ca2+-activated K+ channel blocker) completely prevented the vasodilatory action of Boldine at all doses tested. Together, the present study showed the renal vasodilatory properties of Boldine, an effect dependent on the generation of nitric oxide and the opening of a small-conductance Ca2+-activated K+ channel.
Boldine Attenuates Synaptic Failure and Mitochondrial Deregulation in Cellular Models of Alzheimer's Disease
Front Neurosci 2021 Feb 19;15:617821.PMID:33679301DOI:10.3389/fnins.2021.617821.
Alzheimer's disease (AD) is the most common cause of senile dementia worldwide, characterized by both cognitive and behavioral deficits. Amyloid beta peptide (Aβ) oligomers (AβO) have been found to be responsible for several pathological mechanisms during the development of AD, including altered cellular homeostasis and synaptic function, inevitably leading to cell death. Such AβO deleterious effects provide a way for identifying new molecules with potential anti-AD properties. Available treatments minimally improve AD symptoms and do not extensively target intracellular pathways affected by AβO. Naturally-derived compounds have been proposed as potential modifiers of Aβ-induced neurodysfunction and cytotoxicity based on their availability and chemical diversity. Thus, the aim of this study was to evaluate Boldine, an alkaloid derived from the bark and leaves of the Chilean tree Peumus boldus, and its capacity to block some dysfunctional processes caused by AβO. We examined the protective effect of Boldine (1-10 μM) in primary hippocampal neurons and HT22 hippocampal-derived cell line treated with AβO (24-48 h). We found that Boldine interacts with Aβ in silico affecting its aggregation and protecting hippocampal neurons from synaptic failure induced by AβO. Boldine also normalized changes in intracellular Ca2+ levels associated to mitochondria or endoplasmic reticulum in HT22 cells treated with AβO. In addition, Boldine completely rescued the decrease in mitochondrial membrane potential (ΔΨm) and the increase in mitochondrial reactive oxygen species, and attenuated AβO-induced decrease in mitochondrial respiration in HT22 hippocampal cells. We conclude that Boldine provides neuroprotection in AD models by both direct interactions with Aβ and by preventing oxidative stress and mitochondrial dysfunction. Additional studies are required to evaluate the effect of Boldine on cognitive and behavioral deficits induced by Aβ in vivo.
Boldine Ameliorates Estrogen Deficiency-Induced Bone Loss via Inhibiting Bone Resorption
Front Pharmacol 2018 Sep 13;9:1046.PMID:30271347DOI:10.3389/fphar.2018.01046.
Osteoporosis is an enormous health problem caused by the imbalance between bone resorption and bone formation. The current therapeutic strategies for osteoporosis still have some limitations. Boldine, an alkaloid isolated from Peumus boldus, has been shown to have antioxidant and anti-inflammatory effects in vivo. For the first time, we discover that Boldine has a protective effect for the estrogen deficiency-induced bone loss in mice. According to the Micro-CT and histomorphometry assays, Boldine conducts this protective effect through inhibiting bone resorption without affecting bone formation in vivo. Moreover, we showed that Boldine can inhibit receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation via impairing the AKT signaling pathways, while SC79 (an AKT agonist) partially rescue this effect. In conclusion, our results suggest that Boldine can prevent estrogen deficiency-induced osteoporosis by inhibiting osteoclastogenesis. Thus, Boldine may be served as a novel therapeutic agent for anti-osteoporotic therapy.