Asperosaponin VI
(Synonyms: 川续断皂苷 VI) 目录号 : GC60603
A triterpenoid saponin with diverse biological activities
Cas No.:39524-08-8
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
Asperosaponin VI is a triterpenoid saponin that has been found in D. asper and has diverse biological activities.1,2,3 It increases bone morphogenetic protein 2 (BMP2) levels in, and induces differentiation of, MC3T3-E1 mouse preosteoblasts in a concentration-dependent manner.1 It also inhibits osteoclast formation induced by RANKL in vitro and reduces joint inflammation and bone loss in a mouse model of collagen-induced arthritis when administered at a dose of 20 mg/kg.2 Asperosaponin VI (150 and 450 mg/kg) reduces increases in acetic acid-induced vascular permeability and increases the latency to paw withdrawal in the hot plate test in mice.3
1.Niu, Y., Li, Y., Huang, H., et al.Asperosaponin VI, a saponin component from Dipsacus asper wall, induces osteoblast differentiation through bone morphogenetic protein-2/p38 and extracellular signal-regulated kinase 1/2 pathwayPhytother. Res.25(11)1700-1706(2011) 2.Liu, K., Liu, Y., Xu, Y., et al.Asperosaponin VI protects against bone destructions in collagen induced arthritis by inhibiting osteoclastogenesisPhytomedicine63153006(2019) 3.Gong, L.-L., Yang, S., Liu, H., et al.Anti-nociceptive and anti-inflammatory potentials of Akebia saponin DEur. J. Pharmacol.84585-90(2019)
| Cas No. | 39524-08-8 | SDF | |
| 别名 | 川续断皂苷 VI | ||
| Canonical SMILES | O[C@@H]1[C@H](O)[C@@H](O)[C@]([H])(O[C@@H]2[C@@](C)(CO)[C@@](CC[C@]3(C)[C@]4([H])CC=C5[C@@]3(C)CC[C@]6(C(O[C@@H]7O[C@H](CO[C@H]8[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O8)[C@@H](O)[C@H](O)[C@H]7O)=O)[C@@]5([H])CC(C)(C)CC6)([H])[C@]4(C)CC2)OC1 | ||
| 分子式 | C47H76O18 | 分子量 | 929.1 |
| 溶解度 | DMSO: 100 mg/mL (107.63 mM) | 储存条件 | -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 | 1.0763 mL | 5.3816 mL | 10.7631 mL |
| 5 mM | 0.2153 mL | 1.0763 mL | 2.1526 mL |
| 10 mM | 0.1076 mL | 0.5382 mL | 1.0763 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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Asperosaponin VI ameliorates the CMS-induced depressive-like behaviors by inducing a neuroprotective microglial phenotype in hippocampus via PPAR-γ pathway
J Neuroinflammation 2022 May 24;19(1):115.PMID:35610721DOI:10.1186/s12974-022-02478-y.
Background: The natural compound Asperosaponin VI has shown potential as an antidepressant, but how it works is unclear. Here, we explored its effects on mice exposed to chronic mild stress (CMS) and the underlying molecular pathways. Methods: Mice were exposed to CMS for 3 weeks followed by Asperosaponin VI (40 mg/kg) or imipramine (20 mg/kg) for another 3 weeks. Depression-like behaviors were assessed in the forced swimming test (FST), sucrose preference test (SPT), tail suspension test (TST). Microglial phenotypes were evaluated using immunofluorescence staining, real-time quantitative PCR and enzyme-linked immunosorbent assays in hippocampus of mice. In some experiments, stressed animals were treated with the PPAR-γ antagonist GW9662 to examine its involvement in the effects of Asperosaponin VI. Blockade of PPAR-γ in asperosaponin VI-treated primary microglia in the presence of lipopolysaccharide (LPS) was executed synchronously. The nuclear transfer of PPAR-γ in microglia was detected by immunofluorescence staining in vitro and in vivo. A co-cultured model of neuron and microglia was used for evaluating the regulation of ASA VI on the microglia-neuron crosstalk molecules. Results: Asperosaponin VI ameliorated depression-like behaviors of CMS mice based on SPT, TST and FST, and this was associated with a switch of hippocampal microglia from a pro-inflammatory (iNOS+-Iba1+) to neuroprotective (Arg-1+-Iba1+) phenotype. CMS reduced the expression levels of PPAR-γ and phosphorylated PPAR-γ in hippocampus, which Asperosaponin VI partially reversed. GW9662 treatment prevented the nuclear transfer of PPAR-γ in asperosaponin VI-treated microglia and inhibited the induction of Arg-1+ microglia. Blockade of PPAR-γ signaling also abolished the ability of Asperosaponin VI to suppress pro-inflammatory cytokines while elevating anti-inflammatory cytokines in the hippocampus of CMS mice. The Asperosaponin VI also promoted interactions between hippocampal microglia and neurons by enhancing CX3CL1/CX3CR1 and CD200/CD200R, and preserved synaptic function based on PSD95, CamKII β and GluA levels, but not in the presence of GW9662. Blockade of PPAR-γ signaling also abolished the antidepressant effects of Asperosaponin VI in the SPT, TST and FST. Conclusion: CMS in mice induces a pro-inflammatory microglial phenotype that causes reduced crosstalk between microglia and neuron, inflammation and synaptic dysfunction in the hippocampus, ultimately leading to depression-like behaviors. Asperosaponin VI may ameliorate the effects of CMS by inducing microglia to adopt a PPAR-γ-dependent neuroprotective phenotype.
Therapeutic effects of Asperosaponin VI in rabbit tendon disease
Regen Ther 2022 Mar 3;20:1-8.PMID:35310016DOI:10.1016/j.reth.2022.02.001.
Introduction: This study explored the effects and molecular mechanisms of Asperosaponin VI in tendon disease. Methods: Forty-eight purebred adult male New Zealand white rabbits were randomly divided into the normal group (normal, n = 8); saline group (saline, n = 8) and prostaglandin E2 group (n = 32), which was further divided into four subgroups that were treated with Asperosaponin VI doses of 0 mg/kg (model, n = 8), 10 mg/kg (10, n = 8), 20 mg/kg (20, n = 8) and 40 mg/kg (40, n = 8). The expression levels of matrix metallopeptidase 1 (MMP1), metallopeptidase inhibitor 1 (TIMP1), transforming growth factor beta 1 (TGFB1), serpin family E member 1 (SERPINE1), collagen Ⅰ (COL1), collagen Ⅲ (COL3) and tenomodulin (TNMD) in Achilles tendon tissue were determined through Western blot analysis. The histopathological changes in tendon tissue were observed by using Masson staining and haematoxylin-eosin staining. Results: The expression levels of MMP1, TIMP1 and COL3 were higher and those of TGFB1, SERPINE1, COL1 and TNMD were lower in the 0 mg/kg group than in the normal group (P < 0.05). Compared with those in the 0 mg/kg group, the levels of MMP1 were lower in the 20 and 40 mg/kg groups. Compared with those in the 0 mg/kg group, the levels of TIMP1 were lower and the levels of TGFB1, COL1 and TNMD were higher in the 10, 20 and 40 mg/kg groups. In addition, compared with those in other groups, the levels of SERPINE1 in the 40 mg/kg group were significantly higher and the levels of COL3 in the 10 and 20 mg/kg groups were significantly lower (P < 0.05). Fibrous tissue arrangements and structures in the 40 mg/kg group were similar to those in the control group. Conclusion: The effects of Asperosaponin VI on injured tendons mainly involve eliminating inflammation, restoring balance to extracellular matrix collagen metabolism and inducing tendon cell proliferation. Asperosaponin VI is likely to be an ideal drug for the prevention and treatment of tendon disease.
Asperosaponin VI stimulates osteogenic differentiation of rat adipose-derived stem cells
Regen Ther 2019 May 10;11:17-24.PMID:31193169DOI:10.1016/j.reth.2019.03.007.
In the aging population, the decrease on osteogenic differentiation resulted into a significant reduction in bone formation. Bone tissue engineering has been a successful technique for treatment of bone defects. It is reported that adipose-derived stem cells (ADSCs) have pluripotency to differentiate into adipocytes and osteoblasts. However little is revealed about the effect of the herbal medicine Asperosaponin VI (ASA VI) on ADSCs differentiation. In our study, we isolated and identified ADSCs from rats. We examined the effect of different concentrations of ASA VI in ADSCs on alkaline phosphatase (ALP) activity, calcium deposition, the expression of bone-related proteins and the release of inflammatory cytokines. Flowcytometry assay showed ADSCs were highly expressed CD44 and CD105, but hardly expressed CD34 and CD45, suggesting ADSCs were successfully isolated for follow-up experiments. ALP activity examination and Alizarin red (AR) stain showed that ASA VI enhanced the ALP activity and promoted matrix mineralization in ADSCs. In addition, bone-related protein OCN and RUNX2, and Smad2/3 phosphorylation was upregulated after ASA VI treatment in ADSCs. ELISA results showed that ASA VI blocked the release of TNF-α, IL-6 and IL-1β in ADSCs. Considering this results, we concluded that ASA VI promotes osteogenic differentiation of ADSCs through inducing the expression of bone-related proteins. These findings enriched the function of ASA VI as a regenerative medicine and shed new light for the treatment of bone defects in clinical research.
Asperosaponin VI Injection Enhances Orthodontic Tooth Movement in Rats
Med Sci Monit 2020 Apr 23;26:e922372.PMID:32323648DOI:10.12659/MSM.922372.
BACKGROUND This study was performed to investigate the effect of local injection of Asperosaponin VI (ASA VI) on the orthodontic tooth movement in rats. MATERIAL AND METHODS A total of 64 healthy female Sprague-Dawley rats were selected and divided into 2 groups randomly: the ASA VI group and the control group. For the ASA VI group, 10 mg/kg ASA VI solution was injected into buccal submucoperiosteal of bilaterally first maxillary molars, and the same volume of normal saline was given to the control group. The orthodontic force was applied to the maxillary first molars. All rats were sacrificed on days 3, 7, or 14. Tooth movement effects on the periodontium were analyzed through hematoxylin and eosin (H&E) staining, tartrate-resistant acid phosphatase (TRAP) staining and immunohistochemistry analysis. Tooth movement measurements and alveolar bone volumetric changes were analyzed using a micro-computed tomography (CT) scan. Molecular changes were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. RESULTS The ASA VI group presented with a significant increase of tooth movement, osteoclast number, and the expression of osteoclast differentiation factor (ODF) compared with the control group. ASA VI also induced a significant decrease in bone volume and density and an increase in trabecular spacing and RANKL (receptor activator of nuclear factor kappa-B ligand) expression at the compression side. Furthermore, ASA VI stimulated bone formation on the tension side by enhancing OCN (osteocalcin) expression and RUNX2 (runt-related transcription factor 2) expression, increasing bone volume and density and decreasing in trabecular spacing. CONCLUSIONS Injection of ASA VI may accelerate tooth movement via increasing the activity of osteoclasts, stimulating bone resorption at the compression side. Furthermore, ASA VI has a positive effect on bone formation at the tension side.
Asperosaponin VI induces osteogenic differentiation of human umbilical cord mesenchymal stem cells via the estrogen signaling pathway
Medicine (Baltimore) 2022 Dec 16;101(50):e32344.PMID:36550906DOI:10.1097/MD.0000000000032344.
Background: Asperosaponin VI (ASA VI) is an active ingredient found in the traditional Chinese herb Radix Dipsaci, which is used to treat fractures. ASA VI combined with osteogenic medium can induce osteogenic differentiation of rat-derived stem cells. However, whether ASA VI alone can induce osteoblast differentiation of human mesenchymal stem cells (MSCs) remains unclear. Methods: ASA VI human-derived binding proteins were searched in the PharmMapper database, osteogenesis-related signaling pathways were obtained through a literature search, and proteins contained in these signaling pathways were queried in the Kyoto Encyclopedia of Genes and Genomes database. SystemsDock was used to perform online molecular docking of target proteins to evaluate their binding abilities, and validation experiments were performed. Results: A total of 620 ASA VI target proteins and 12 osteogenesis-related signaling pathways were queried, and 17 intersecting targets were screened. Molecular docking results showed that these targets had high binding affinity for ASA VI. We selected estrogen receptor 2 and its estrogen signaling pathway for experimental validation. The results showed that ASA VI can induce the osteogenic differentiation of MSCs through the estrogen signaling pathway. Conclusion: ASA VI can independently induce osteogenic differentiation of human umbilical cord MSCs, and the estrogen signaling pathway plays an important role in this process. Thus, ASA VI may have potential as an anti-osteoporosis drug.