Bacopaside I
(Synonyms: 假马齿苋皂苷I) 目录号 : GC35457
A saponin with diverse biological activities
Cas No.:382148-47-2
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
Bacopaside I is a saponin that has been found in B. monniera and has diverse biological activities.1,2,3,4 It inhibits monoamine oxidase A (MAO-A) and MAO-B (IC50s = 17.08 and 94.22 ?g/ml, respectively).1 Bacopaside I (5, 15, and 50 mg/kg) decreases immobility time in the tail suspension and forced swim tests, as well as brain malondialdehyde (MDA) levels, and increases brain superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities in mice.2 It increases time spent in the target quadrant in the Morris water maze and reduces amyloid plaque formation in the APP/PS1 transgenic mouse model of Alzheimer’s disease.3 Bacopaside I (3, 10, and 30 mg/kg) reduces cerebral edema and infarct volume in a rat model of transient focal ischemia induced by middle cerebral artery occlusion.4
1.Singh, R., Ramakrishna, R., Bhateria, M., et al.In vitro evaluation of Bacopa monniera extract and individual constituents on human recombinant monoamine oxidase enzymesPhytother. Res.28(9)1419-1422(2014) 2.Liu, X., Liu, F., Yue, R., et al.The antidepressant-like effect of bacopaside I: Possible involvement of the oxidative stress system and the noradrenergic systemPharmacol. Biochem. Behav.110224-230(2013) 3.Li, Y., Yuan, X., Shen, Y., et al.Bacopaside I ameliorates cognitive impairment in APP/PS1 mice via immune‐mediated clearance of β‐amyloidAging (Albany NY)8(3)521-533(2016) 4.Liu, X., Yue, R., Zhang, J., et al.Neuroprotective effects of bacopaside I in ischemic brain injuryRestor. Neurol. Neurosci.31(2)109-123(2013)
| Cas No. | 382148-47-2 | SDF | |
| 别名 | 假马齿苋皂苷I | ||
| 分子式 | C46H74O20S | 分子量 | 979.13 |
| 溶解度 | DMSO : 100 mg/mL (102.13 mM; Need ultrasonic) | 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 | 1.0213 mL | 5.1066 mL | 10.2131 mL |
| 5 mM | 0.2043 mL | 1.0213 mL | 2.0426 mL |
| 10 mM | 0.1021 mL | 0.5107 mL | 1.0213 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 |
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| % 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。
Insights Into the Molecular Aspects of Neuroprotective Bacoside A and Bacopaside I
Curr Neuropharmacol 2019;17(5):438-446.PMID:29676230DOI:10.2174/1570159X16666180419123022.
Bacopa monnieri, commonly known as Brahmi, has been extensively used as a neuromedicine for various disorders such as anxiety, depression and memory loss. Chemical characterization studies revealed the major active constituents of the herb as the triterpenoid saponins, bacosides. Bacoside A, the vital neuroprotective constituent, is composed of four constituents viz., bacoside A3, bacopaside II, jujubogenin isomer of bacopasaponin C (bacopaside X) and bacopasaponin C. B. monnieri extracts as well as bacosides successfully establish a healthy antioxidant environment in various tissues especially in the liver and brain. Free radical scavenging, suppression of lipid peroxidation and activation of antioxidant enzymes by bacosides help to attain a physiological state of minimized oxidative stress. The molecular basis of neuroprotective activity of bacosides is attributed to the regulation of mRNA translation and surface expression of neuroreceptors such as AMPAR, NMDAR and GABAR in the various parts of the brain. Bioavailability as well as binding of neuroprotective agents (such as bacosides) to these receptors is controlled by the Blood Brain Barrier (BBB). However, nano conversion of these drug candidates easily resolves the BBB restriction and carries a promising role in future therapies. This review summarizes the neuroprotective functions of B. monnieri extracts as well as its active compounds (bacoside A, Bacopaside I) and the molecular mechanisms responsible for these pharmacological activities.
Immunochromatographic determination of Bacopaside I in biological samples
J Chromatogr B Analyt Technol Biomed Life Sci 2017 Jan 1;1040:60-66.PMID:27907870DOI:10.1016/j.jchromb.2016.11.022.
We describe a novel immunochromatographic method for qualitative and quantitative analyses of Bacopaside I, a bioactive constituent in Bacopa monnieri (L.) Wettst in biological samples. The assay was performed on polyethersulfone membrane using a polyclonal antibody raised against Bacopaside I. The finalised method could quantitatively determine Bacopaside I in the range of 31.3-1000.0ng and the detection and quantification limits were 1.0 and 31.3ng, respectively. The percentage recoveries of Bacopaside I in blood and urine were nearly 100% indicating the accuracy of the extraction. The method was then applied for the determination of this compound in rat serum, urine and feces after an oral dose of 15mg/kg body weight. About 4% of the ingested dose of Bacopaside I was detected in rat feces but none was detected in serum and urine which accorded with results from liquid chromatography tandem mass spectrometry. The accuracy, selectivity, sensitivity of the method are appropriate for in vivo pharmacokinetic studies.
Bacopaside I ameliorates cognitive impairment in APP/PS1 mice via immune-mediated clearance of β-amyloid
Aging (Albany NY) 2016 Mar;8(3):521-33.PMID:26946062DOI:10.18632/aging.100913.
Standardized extracts of Bacopa monniera (BME) have been shown to exert a neuroprotective effect against mental diseases, such as depression, anxiety and Alzheimer's disease (AD), in chronic administration studies. However, its mechanism of action has remained unclear. In this study, we evaluated the therapeutic effect of Bacopaside I (BS-I), a major triterpenoid saponin of BME, on the cognitive impairment and neuropathology in APP/PS1 transgenic mice and explored the possible mechanism from a biological systems perspective. We found that BS-I treatment significantly ameliorated learning deficits, improved long-term spatial memory, and reduced plaque load in APP/PS1 mice. We constructed BS-I's therapeutic effect network by mapping the nodes onto the protein-protein interaction (PPI) network constructed according to their functional categories based on genomic and proteomic data. Because many of the top enrichment categories related to the processes of the immune system and phagocytosis were detected, we proposed that BS-I promotes amyloid clearance via the induction of a suitable degree of innate immune stimulation and phagocytosis. Our research may help to clarify the neuroprotective effect of BME and indicated that natural saponins target the immune system, which may offer new research avenues to discover novel treatments for AD.
Neuroprotective effects of Bacopaside I in ischemic brain injury
Restor Neurol Neurosci 2013;31(2):109-23.PMID:23160060DOI:10.3233/RNN-120228.
Purpose: Bacopa monnieri (L.) WETTST. is extensively used in traditional Indian medicine as a nerve tonic. The neuropharmacological properties of Bacopaside I, an important component from B. monnieri, have not been studied so far. The present study investigated the effects and possible mechanisms of Bacopaside I in a rat model of transient focal ischemia induced by middle cerebral artery occlusion (MCAO). Methods: Adult male Sprague-Dawley rats were divided into five groups: sham-operated group, ischemia group, and three bacopaside I-treated groups (3, 10 and 30 mg/kg) respectively. Bacopaside I or vehicle (0.5% CMC-Na) was administered orally once a day for 6 days. On the third day, the rats were subjected to 2 h right MCAO via the intraluminal filament technique and 70 h reperfusion. Assessment of behavioral deficits both at 22 and 70 h, and measurement of cerebral infarct volume, edema, cerebral energy metabolism, relative enzyme activities, malondialdehyde (MDA) content, nitric oxide (NO) level, and antioxidant enzyme activities at 70 h, performed after MCAO reperfusion. Results: Bacopaside I (10 and 30 mg/kg) treatment produced significant reduction in neurological deficits at 22 and 70 h, and significantly reduced cerebral infarct volume and edema at 70 h, when compared with the ischemia group. Animal, that were orally treated with Bacopaside I (3, 10 and 30 mg/kg) showed increased the brain ATP content, energy charge (EC), total adenine nucleotides (TAN), nitric oxide (NO) level, Na+K+ATPase and Ca2+Mg2+ATPase activity. Bacopaside I (3, 10 and 30 mg/kg) treatment also improved antioxidant enzyme activities including brain superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), in varying degrees, compared with the ischemia group. In addition, three doses of Bacopaside I (3, 10 and 30 mg/kg) markedly inhibited the increase in MDA content of the brain. Conclusions: These findings indicated that Bacopaside I possess a neuroprotective effect against injury caused by cerebral ischemia. The protective mechanism might be related to improving cerebral energy metabolism and increasing antioxidant levels.
Analysis of Bacopaside I in biomatrices using liquid chromatography-tandem mass spectrometry: Pharmacokinetics and brain distribution in Swiss-albino mice
J Pharm Biomed Anal 2016 Jun 5;125:101-9.PMID:27017568DOI:10.1016/j.jpba.2016.03.002.
Bacopaside I (BP-I) is the major pseudojujubogenin glycoside of Bacopa monniera (BM) extract which has been widely used as a nerve tonic to improve the memory and intellect of human beings from ancient times. A selective and sensitive liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for the quantification of BP-I in mouse plasma and brain homogenate has been developed and validated. All biosamples were processed by liquid-liquid extraction and chromatographed on C18- reversed phase column using mobile phase consisting of ammonium acetate (10mM, pH 4) - acetonitrile (10:90, v/v) at a flow rate of 0.5mL/min. The detection was performed in negative electrospray ionization mode and the precursor/product ion transitions of BP-I and internal standard (IS) hydrochlorothiazide were quantified in multiple reaction monitoring (MRM) using QTRAP-5500 MS/MS. The linearity was established over the concentration range of 0.5-2000ng/mL (r(2)>0.990), with lower limit of quantification (LLOQ) of 0.5ng/mL in both plasma and brain matrix. Within- and between-run precision and accuracy were well within the acceptable limits of variation. Consistent and reproducible recovery (>70%) was obtained with insignificant matrix effect for BP-I and IS. The method fulfilled US Food and Drug Administration (USFDA) guidelines for bioanalytical method validation in terms of selectivity, sensitivity, linearity, accuracy, precision, matrix effect, dilution integrity, carry-over effect and stability. Further, the method was successfully applied to execute the plasma pharmacokinetics and brain distribution of BP-I in Swiss-albino mice following intravenous administration at a dose of 5mg/kg.