Araloside A
(Synonyms: 木皂苷A,Chikusetsusaponin IV) 目录号 : GC35380
A triterpenoid saponin with anti-inflammatory and gastroprotective activities
Cas No.:7518-22-1
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
Araloside A is a triterpenoid saponin that has been found in A. taibaiensis and has anti-inflammatory and gastroprotective effects.1,2 It increases apoptosis of and decreases production of IL-1β and IL-6 in human MH7A rheumatoid arthritis fibroblast-like synoviocytes when used at concentrations ranging from 4 to 16 ?M.1 Araloside A (50 and 100 mg/kg) reduces gastric acid secretion and lesion size in rat models of hydrochloric acid and ethanol-, aspirin-, water immersion stress-, or pyloric ligation-induced ulcer formation.2
1.Ding, Y., Zhao, Q., and Wang, L.Pro-apoptotic and anti-Inflammatory effects of araloside A on human rheumatoid arthritis fibroblast-like synoviocytesChem. Biol. Interact.306131-137(2019) 2.Lee, E.B., Kim, O.J., Kang, S.S., et al.Araloside A, an antiulcer constituent from the root bark of Aralia elataBiol. Pharm. Bull.28(3)523-526(2005)
| Cas No. | 7518-22-1 | SDF | |
| 别名 | 木皂苷A,Chikusetsusaponin IV | ||
| Canonical SMILES | O=C([C@]1(CCC(C)(C)C2)[C@]2([H])C3=CC[C@@]4([H])[C@@](C)(CC[C@]5([H])[C@@]4(CC[C@H](O[C@]([C@@H]([C@@H](O)[C@@H]6O[C@]7([H])O[C@@H](CO)[C@H](O)[C@H]7O)O)([H])O[C@@H]6C(O)=O)C5(C)C)C)[C@]3(C)CC1)O[C@@H]([C@@H]([C@@H](O)[C@@H]8O)O)O[C@@H]8CO | ||
| 分子式 | C47H74O18 | 分子量 | 927.08 |
| 溶解度 | PBS (pH 7.2): 5 mg/ml | 储存条件 | 4°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 | 1.0787 mL | 5.3933 mL | 10.7866 mL |
| 5 mM | 0.2157 mL | 1.0787 mL | 2.1573 mL |
| 10 mM | 0.1079 mL | 0.5393 mL | 1.0787 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。
[Tissue distribution of Araloside A in rats]
Zhongguo Zhong Yao Za Zhi 2017 Oct;42(20):4002-4006.PMID:29243440DOI:10.19540/j.cnki.cjcmm.20170901.011.
Araloside A is one of the main active ingredients of Aralia taibaiensis. In this study, HPLC-MS/MS analysis method of Araloside A in the main organs of SD rats was established. At the same time, the content of Araloside A in the main organs (heart, liver, spleen, lung, kidney, brain) after oral administration with Araloside A (50 mg•kg⁻¹) were determined to explore the tissue distribution characteristics of Araloside A in vivo. The results showed that the methodological study of Araloside A in the main organs of SD rats met the requirements, Araloside A distributed in heart, liver, spleen, lung, kidney and brain tissues reached peak at 1 h or 2 h after oral administration with 50 mg•kg-1.The distributions of Araloside A at different time points after administration were distinct as follows： the content of Araloside A at 20 min：liver>heart>spleen>lung>kidney>brain; the content of Araloside A at 1 h： liver>spleen>kidney>lung>heart>brain; the content of Araloside A at 2 h： liver>kidney>heart>spleen>lung>brain; the content of Araloside A at 4 h： kidney>liver>spleen>heart>lung>brain; the content of Araloside A at 8 h： spleen>heart>liver>kidney>lung>brain. Therefore, Araloside A was mainly distributed in liver tissue, which had a certain correlation with the common use of Aralia taibaiensis in the treatment of hepatic disease. In addition, Araloside A shows a low content but an obvious distribution in brain tissues, which indicates that the drug can pass through blood-brain barrier, and provides the basis for the study of Araloside A in brain tissue.
Synergistic Antioxidant Effects of Araloside A and L-Ascorbic Acid on H2O2-Induced HEK293 Cells: Regulation of Cellular Antioxidant Status
Oxid Med Cell Longev 2021 Jul 9;2021:9996040.PMID:34336129DOI:10.1155/2021/9996040.
Araloside A is a pentacyclic triterpenoid saponin, and L-ascorbic acid is a globally recognized antioxidant. In this study, coadministered Araloside A and L-ascorbic acid were found to have a strong synergistic antioxidant effect, and correlations between cellular antioxidant indexes and free radical scavenging ability were found. Individual and combined pretreatment with Araloside A and L-ascorbic acid increased both cell viability and antioxidant enzyme activity and inhibited the release of lactate dehydrogenase (LDH); the accumulation of malondialdehyde (MDA), lipid peroxidation (LPO) products, and H2O2; and the production of intracellular reactive oxygen species (ROS), protein carbonyls, and 8-hydroxy-2-deoxy guanosine (8-OHdG). Free radical scavenging ability was positively correlated with superoxide dismutase (SOD) and catalase (CAT) activity, the glutathione (GSH)/oxidized glutathione (GSSG) ratio, and total antioxidant capacity (T-AOC). Our study is the first investigation of Araloside A and L-ascorbic acid coadministration for the treatment of diseases caused by oxidative stress. The synergistic antioxidant effects of Araloside A and L-ascorbic acid support their potential as functional food ingredients for the elimination of oxidative stress-induced adverse reactions.
Pro-apoptotic and anti-inflammatory effects of Araloside A on human rheumatoid arthritis fibroblast-like synoviocytes
Chem Biol Interact 2019 Jun 1;306:131-137.PMID:31004595DOI:10.1016/j.cbi.2019.04.025.
Rheumatoid arthritis fibroblast-like synoviocytes play an essential role in the occurrence and progression of rheumatoid arthritis. As the main pharmacologically active components of Aralia taibaiensis, total saponins, particularly triterpenoid saponins, have been shown to possess multiple pharmacological activities including relieving rheumatism. However, the effect of Araloside A, a triterpenoid saponin extracted from the root bark of Aralia taibaiensis, on rheumatoid arthritis remains unknown. Cell counting kit-8 assay was employed to determine cell viability. Flow cytometry analysis, caspase-3/7 activity assay and Western blot analysis of cytochrome c and B-cell lymphoma 2 were conducted to evaluate cell apoptosis. Inflammation was assessed by detecting the production of inflammatory cytokines including interleukin-6 and interleukin-8, as well as inflammatory mediators including nitric oxide and prostaglandin E2. The changes of the nuclear factor kappa B pathway were examined by Western blot. Results showed that Araloside A concentration-dependently inhibited the proliferation of MH7A cells. Meanwhile, Araloside A dose-dependently augmented the apoptotic rate and caspase-3/7 activity, increased cytochrome c level and decreased B-cell lymphoma 2 level in MH7A cells. Araloside A concentration-dependently curbed the production of interleukin-6, interleukin-8, prostaglandin E2 and nitric oxide in MH7A cells. In addition, we found that Araloside A inhibited the nuclear factor kappa B pathway and inhibition of the nuclear factor kappa B pathway by BAY11-7082 and PDTC showed a similar role to Araloside A in MH7A cells. Taken together, Araloside A exerted pro-apoptotic and anti-inflammatory effects in rheumatoid arthritis fibroblast-like synoviocytes via inhibition of the nuclear factor kappa B pathway.
Intestinal absorption mechanisms of Araloside A in situ single-pass intestinal perfusion and in vitro Caco-2 cell model
Biomed Pharmacother 2018 Oct;106:1563-1569.PMID:30119231DOI:10.1016/j.biopha.2018.07.117.
Araloside A is a triterpenoid saponin,which exhibits a broad spectrum of pharmacological activities, such as stimulating fibrinolysis, preventing coagulant, inhibiting renin, and decreasing blood pressure. Our previous report found that the compound exhibits a poor absolute bioavailability. However the underlying mechanisms of its absorption have not been investigated in the small intestine or in a Caco-2 cell model. In this study, the absorption mechanisms of Araloside A were investigated in a Caco-2 cell monolayer and in a single-pass intestinal perfusion in situ model with Sprague-Dawley rats. The effects of basic parameters, such as compound concentration, time, temperature, paracellular pathway, different intestinal segments were analyzed, and the susceptibility of Araloside A absorption process to treatment with various inhibitors, such as the P-gp inhibitor verapamil, the multidrug resistance protein2 inhibitors (MRP2) MK571 and indomethacin, the breast cancer resistance protein (BCRP) inhibitors Ko143 and reserpine, and endocytosis inhibitor chlorpromazine were assessed. It can be found that the mechanisms of intestinal absorption of Araloside A may involve multiple transport pathways, such as passive diffusion, the paracellular pathway, as well as the participation of efflux transporters.
Gastroprotective effect of Araloside A on ethanol- and aspirin-induced gastric ulcer in mice: involvement of H+/K+-ATPase and mitochondrial-mediated signaling pathway
J Nat Med 2019 Mar;73(2):339-352.PMID:30523551DOI:10.1007/s11418-018-1256-0.
The aim of this study was to elucidate the gastroprotective activity and possible mechanism of involvement of Araloside A (ARA) against ethanol- and aspirin-induced gastric ulcer in mice. The experimental mice were randomly divided into control, model, omeprazole (20 mg/kg, orally) and ARA (10, 20 and 40 mg/kg, orally). Gastric ulcer in mice was induced by intragastric administration of 80% ethanol (10 mL/kg) containing 15 mg/mL aspirin 4 h after drug administration on day 7. The results indicated that ARA could significantly raise gastric juice volume and acidity; ameliorate gastric mucosal blood flow, gastric binding mucus volume, ulcer index and ulcer inhibition rate; suppress H+/K+-ATPase activity, which was confirmed by computer-aided docking simulations; inhibit the release of mitochondrial cytochrome c into the cytoplasm; inhibit caspase-9 and caspase-3 activities and down-regulate mRNA expression levels; down-regulate the mRNA and protein expressions of apoptosis protease-activating factor-1 and protein expression of cleaved poly(ADP ribose) polymerase-1; and up-regulate Bcl-2 mRNA and protein expressions and down-regulate Bax mRNA and protein expressions, thus elevating the Bcl-2/Bax ratio in a dose-dependent manner. Histopathological observations further provided supportive evidence for the aforementioned results. The results demonstrated that ARA exerted beneficial gastroprotective effects on alcohol- and aspirin-induced gastric ulcer in mice, which was related to suppressing H+/K+-ATPase activity as well as pro-apoptotic protein expression, and promoting anti-apoptotic protein expression, thus alleviating gastric mucosal injury and cell death.