Tenuifoliside A
(Synonyms: 细叶远志苷A) 目录号 : GC39074
Tenuifoliside A 分离自远志，具有抗凋亡和抗抑郁作用。在 C6 细胞中，Tenuifoliside A 表现出其神经营养作用，并通过 ERK/CREB/BDNF 信号通路促进细胞增殖。
Cas No.:139726-35-5
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
Tenuifoliside A is isolated from Polygala tenuifolia, has anti-apoptotic and antidepressant-like effects. Tenuifoliside A exhibits its neneurotrophic effects and promotes cell proliferation through the ERK/CREB/BDNF signal pathway in C6 cells[1].
[1]. Dong XZ, et al. Effect of Tenuifoliside A isolated from Polygala tenuifolia on the ERK and PI3K pathways in C6 glioma cells. Phytomedicine. 2014 Sep 15;21(10):1178-88.
| Cas No. | 139726-35-5 | SDF | |
| 别名 | 细叶远志苷A | ||
| Canonical SMILES | OC[C@@]1([C@H]([C@H](O)[C@@H](CO)O1)OC(/C=C/C2=CC(OC)=C(OC)C(OC)=C2)=O)O[C@@H]3O[C@@H]([C@@H](O)[C@H](O)[C@H]3O)COC(C4=CC=C(O)C=C4)=O | ||
| 分子式 | C31H38O17 | 分子量 | 682.62 |
| 溶解度 | DMSO : 100 mg/mL (146.49 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 | 1.4649 mL | 7.3247 mL | 14.6494 mL |
| 5 mM | 0.293 mL | 1.4649 mL | 2.9299 mL |
| 10 mM | 0.1465 mL | 0.7325 mL | 1.4649 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。
Tenuifoliside A promotes neurite outgrowth in PC12 cells via the PI3K/AKT and MEK/ERK/CREB signaling pathways
Mol Med Rep 2015 Nov;12(5):7637-42.PMID:26459496DOI:10.3892/mmr.2015.4397.
Previous studies have demonstrated the neuroprotective effect of Tenuifoliside A (TFSA) on corticosterone-induced neuron damage in SH‑SY5Y cells, however, the effect of TFSA on the promotion of neurite outgrowth remains to be elucidated. PC12 cells were treated with TFSA or nerve growth factor, and the levels of proteins were evaluated by western blotting. In addition, for pharmacological experiments, inhibitors of the PD98059 mitogen‑activated protein kinase kinase (MEK) and phosphatidylinositol 3‑kinase (PI3K; LY294002) were added into the culture medium. The present study demonstrated that TFSA significantly increased the percentage of neurite‑bearing cells and promoted neurite extension in PC12 cells. In addition, TFSA‑treated PC12 cells also expressed increased levels of the 43 kD growth‑associated protein (GAP‑43) neural marker, comparable to those in nerve growth factor‑treated cells. The present study also demonstrated that TFSA enhanced the phosphorylation of extracellular signal‑regulated kinase (ERK) and Akt, which are important signaling molecules involved in neural differentiation in PC12 cells. Co‑treatment of the PC12 cells with the PD98059 MEK inhibitor and LY294002 PI3K inhibitor inhibited the neurite outgrowth induced by TFSA. In addition, treatment with TFSA also promoted the phosphorylation of cyclic AMP response element‑binding protein (CREB), which was inhibited completely by treatment with PD98059. In conclusion, the results of the present study demonstrated that TFSA induces neurite extension of PC12 cells and suggested that activation of the MEK/ERK/CREB and PI3K/Akt signaling pathways is involved in this process.
Stable isotope labeling derivatization combined with multiple-mass spectrometry technologies to monitor metabolites of Tenuifoliside A incubated with intestinal bacteria incubation model
Talanta 2021 Mar 1;224:121791.PMID:33379020DOI:10.1016/j.talanta.2020.121791.
Aromatic carboxylic acids (ACAs), play important roles in preventive and therapeutic effects for some diseases. However, complex matrix effect and poor detection sensitivity make it difficult and even rare to detect ACAs in complex bio-samples. Herein, a stable isotope labeling derivatization (SILD) method based on one-pot synthesis of carboxylic amides by aniline (AN) and aniline-d5 (AN-d5) was firstly designed for quantitatively monitoring ACAs under mild conditions. The detection sensitivity was improved up to 500 folds. Importantly, when taking the trace Tenuifoliside A (TA) containing p-hydroxyl-benzoyl- (HB) and 3, 4, 5-trimethoxylcinnamoyl- (TC) unit as a special example via intestinal bacteria incubation, the metabolites ACAs and whole metabolic profiles of TA were firstly accurately and systematically monitored by applying the SILD method combined with multiple-mass spectrometry (MMS) technologies. It provides a convenient, universal, high-sensitivity and high-recovery methodological tool for the systematically metabolic study of trace drugs in vitro and in vivo.
The inhibition of JNK MAPK and NF-κB signaling by Tenuifoliside A isolated from Polygala tenuifolia in lipopolysaccharide-induced macrophages is associated with its anti-inflammatory effect
Eur J Pharmacol 2013 Dec 5;721(1-3):267-76.PMID:24076326DOI:10.1016/j.ejphar.2013.09.026.
The root of Polygala tenuifolia Willd. (Polygalaceae) is well known for its use in the treatment of neurasthenia, amnesia, and inflammation. In this study, we isolated phenyl propanoid type metabolite Tenuifoliside A, one of the phenylpropanoids from P. tenuifolia, and investigated its anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated RAW264.7 and murine peritoneal macrophages. The results showed that Tenuifoliside A inhibited the production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PG E2), and cyclooxygenase (COX)-2. In addition, Tenuifoliside A suppressed the production of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β. We also evaluated the effects of Tenuifoliside A on the activation of nuclear factor-kappaB (NF-κB). Tenuifoliside A inhibited the translocation of the NF-κB subunit p65 into the nucleus by interrupting the phosphorylation and degradation of inhibitor kappa B (IκB)-α in LPS-stimulated murine peritoneal macrophages. Moreover, we confirmed that the suppression of the inflammatory process by Tenuifoliside A was mediated through the mitogen-activated protein kinases (MAPKs) pathway based on the fact that Tenuifoliside A significantly decreased p-c-Jun N-terminal kinase (p-JNK) protein expression in LPS-stimulated murine peritoneal macrophages. Taken together, the anti-inflammatory effects of Tenuifoliside A were mediated by the inhibition of the NF-κB and MAPK pathways. This study is the first report on the anti-inflammatory effects of Tenuifoliside A, and the strong anti-inflammatory effects of Tenuifoliside A provide potential compound to be developed as therapeutic for inflammatory diseases.
Effect of Tenuifoliside A isolated from Polygala tenuifolia on the ERK and PI3K pathways in C6 glioma cells
Phytomedicine 2014 Sep 15;21(10):1178-88.PMID:24877714DOI:10.1016/j.phymed.2014.04.022.
Tenuifoliside A (TFSA) is a bioactive oligosaccharide ester component of Polygala tenuifolia Wild, a traditional Chinese medicine which was used to manage mental disorders effectively. The neuroprotective and anti-apoptotic effects of TFSA have been demonstrated in our previous studies. The present work was designed to study the molecular mechanism of TFSA on promoting the viability of rat glioma cells C6. We exposed C6 cells to TFSA (or combined with ERK, PI3K and TrkB inhibitors) to examine the effects of TFSA on the cell viability and the expression and phosphorylation of key proteins in the ERK and PI3K signaling pathway. TFSA increased levels of phospho-ERK and phospho-Akt, enhanced release of BDNF, which were blocked by ERK and PI3K inhibitors, respectively (U0126 and LY294002). Moreover, the TFSA caused the enhanced phosphorylation of cyclic AMP response element binding protein (CREB) at Ser133 site, the effect was revoked by U0126, LY294002 and K252a. Furthermore, when C6 cells were pretreated with K252a, a TrkB antagonist, known to significantly inhibit the activity of brain-derived neurotrophic factor (BDNF), blocked the levels of phospho-ERK, phospho-Akt and phosphor-CREB. Taking these results together, we suggested the neuroprotection of TFSA might be mediated through BDNF/TrkB-ERK/PI3K-CREB signaling pathway in C6 glioma cells.
Plant-derived natural medicines for the management of depression: an overview of mechanisms of action
Rev Neurosci 2015;26(3):305-21.PMID:25719303DOI:10.1515/revneuro-2014-0058.
Depression is a serious widespread psychiatric disorder that affects approximately 17% of people all over the world. Exploring the neurological mechanisms of the antidepressant activity of plant-derived agents could have a crucial role in developing natural drugs for the management of depression. The aim of the present study is to review the neurological mechanisms of action of antidepressant plants and their constituents. For this purpose, electronic databases, including PubMed, Science Direct, Scopus, and Cochrane Library, were searched from 1966 to October 2013. The results showed that several molecular mechanisms could be proposed for the antidepressant activity of medicinal plants and their constituents. Hypericum species could normalize brain serotonin level. Liquiritin and isoliquiritin from Glycyrrhiza uralensis rhizome act via the noradrenergic system. Rosmarinus officinalis and curcumin from Curcuma longa interact with D1 and D2 receptors as well as elevate the brain dopamine level. Sida tiagii and Aloysia gratissima involve γ-aminobutyric acid and N-methyl-D-aspartate receptors, respectively. Fuzi polysaccharide-1 from Aconitum carmichaeli could affect brain-derived neurotrophic factor signaling pathways. Psoralidin from Psoralea corylifolia seed modulate the hypothalamic-pituitary-adrenal axis. The total glycosides of Paeonia lactiflora demonstrate an inhibitory effect on both subtypes of monoamine oxidase. 3,6'-Di-o-sinapoyl-sucrose and Tenuifoliside A from Polygala tenuifolia exhibit cytoprotective effects on neuronal cells. Further preclinical and clinical trials evaluating their safety, bioefficacy, and bioavailability are suggested to prove the valuable role of natural drugs in the management of depressive disorders.