Rosamultin
(Synonyms: 罗莎白素) 目录号 : GC39068
Rosamultin is a 19 α-hydroxyursane-type triterpenoid isolated from Potentilla anserina L. that inhibits HIV-1 protease. Rosamultin has protective effects on H2O2-induced oxidative damage and apoptosis.
Cas No.:88515-58-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Rosamultin is a 19 α-hydroxyursane-type triterpenoid isolated from Potentilla anserina L. that inhibits HIV-1 protease. Rosamultin has protective effects on H2O2-induced oxidative damage and apoptosis.
[1] Jong Cheol Park, et al. J Med Food. Spring 2005;8(1):107-9. [2] Ling Zhang, et al. Oxid Med Cell Longev. 2018 Jul 16;2018:8415610.
| Cas No. | 88515-58-6 | SDF | |
| 别名 | 罗莎白素 | ||
| Canonical SMILES | OC[C@H]([C@@H](O)[C@H](O)[C@H]1O)O[C@H]1OC([C@]23[C@]([C@](O)([C@H](C)CC3)C)([H])C4=CC[C@@]([C@@]5([C@@](C(C)([C@@H](O)[C@H](O)C5)C)([H])CC6)C)([H])[C@]6(C)[C@]4(C)CC2)=O | ||
| 分子式 | C36H58O10 | 分子量 | 650.84 |
| 溶解度 | Soluble in DMSO | 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 | 1.5365 mL | 7.6824 mL | 15.3648 mL |
| 5 mM | 0.3073 mL | 1.5365 mL | 3.073 mL |
| 10 mM | 0.1536 mL | 0.7682 mL | 1.5365 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。
Rosamultin from Potentilla anserine L. exhibits nephroprotection and antioxidant activity by regulating the reactive oxygen species/C/EBP homologous protein signaling pathway
Phytother Res 2021 Nov;35(11):6343-6358.PMID:34533242DOI:10.1002/ptr.7285.
Rosamultin, a major bioactive constituent from Potentilla anserine L., has antioxidative and hepatoprotective activities. However, its protective effects on cisplatin-induced acute renal injury and the underlying mechanisms remain elusive. In this work, Rosamultin could enhance the viability of HEK293 cells treated by cisplatin. In vivo experiment showed that Rosamultin effectively decreased kidney index, reduced blood urea nitrogen level, decreased urinary protein excretion, and ameliorated the histopathological damage and fibrosis of renal tissue induced by cisplatin. Besides, Rosamultin showed no obvious toxicity in mice. SILAC-based quantitative proteomic analysis identified 4,461 proteins and eight proteins including C/EBP homologous protein (CHOP) were markedly decreased in cisplatin-treated HEK293 cells when exposed to Rosamultin. Biochemical experiments further discovered that Rosamultin could inhibit p38 and JNK activation, and downregulate the levels of CHOP and proteins in its upstream PERK-eIF2α-ATF4 signaling pathway stimulated by cisplatin or tunicamycin. At the same time, Rosamultin reduced the generation of intracellular ROS induced by cisplatin and enhanced the activities of antioxidant enzymes such as SOD, GSH, and CAT. Moreover, Rosamultin markedly suppressed the expression of CHOP, apoptosis-associated proteins, and activation of p38 and JNK in renal tissue. These findings suggest that Rosamultin might be a potential protectant against cisplatin-induced nephrotoxicity.
Rosamultin Attenuates Acute Hypobaric Hypoxia-Induced Bone Injuries by Regulation of Sclerostin and Its Downstream Signals
High Alt Med Biol 2020 Sep;21(3):273-286.PMID:32598190DOI:10.1089/ham.2019.0113.
Wang, Xing-Min, Hui Liu, Jian-Yu Li, Jin-Xia Wei, Xia Li, Yong-Liang Zhang, Ling-Zhi Li, and Xi-Zheng Zhang. Rosamultin attenuates acute hypobaric hypoxia-induced bone injuries by regulation of sclerostin and its downstream signals. High Alt Med Biol. 21:273-286, 2020. Background: Rosamultin, one of the compounds extracted from Potentilla anserina L., exhibited significant pharmacological activity against oxidative stress and hypoxic injury in our previous study. However, the effect of Rosamultin on bone damage induced by acute hypobaric hypoxia (HH) has not been thoroughly studied. Methods: In this study, we first investigated the protective effect of Rosamultin against bone damage in rats following acute exposure to simulated high-altitude hypoxia. Furthermore, we explored the detailed mechanism involved in the regulation of rat bone remodeling by Rosamultin in an acute HH environment through analysis of sclerostin expression and the regulation of downstream signaling pathways. Results: Pretreatment with Rosamultin significantly reduced HH-induced oxidative stress and inflammation, improved bone metabolic abnormalities, and alleviated the imbalance in bone remodeling in rats exposed to acute HH. Rosamultin markedly downregulated the expression of sclerostin, activated the Wnt/β-catenin signaling pathway, and enhanced the ratio of osteoprotegerin/receptor activator of nuclear factor kappa B ligand to maintain the balance of bone formation and resorption. Conclusions: Rosamultin attenuates acute HH-induced bone damage and improves abnormal bone remodeling in rats by inhibition of sclerostin expression and activation of the Wnt/β-catenin signaling pathway.
Protective Effect of Rosamultin against H2O2-Induced Oxidative Stress and Apoptosis in H9c2 Cardiomyocytes
Oxid Med Cell Longev 2018 Jul 16;2018:8415610.PMID:30116494DOI:10.1155/2018/8415610.
Rosamultin is one of the main active compounds isolated from Potentilla anserina L., which belongs to a triterpene compound. Few studies have examined the effect of Rosamultin on oxidative stress and its molecular mechanism. The aim of this present study was to elucidate the protective effect of Rosamultin on H2O2-induced oxidative damage and apoptosis in H9c2 cardiomyocytes and its mechanism. The results showed that the pretreatment of Rosamultin not only increased cell viability but also reduced the release of LDH and CK. Rosamultin inhibited a H2O2-induced decrease in SOD, CAT, and GSH-Px activities and an increase in MDA content. Meanwhile, ROS level, intracellular (Ca2+) fluorescence intensity, and apoptosis rate in the Rosamultin pretreated group were markedly decreased compared with the model group. Rosamultin pretreatment significantly reversed the morphological changes and attenuated H2O2-induced apoptosis. Western blot analysis showed that Rosamultin enhanced the expression of Bcl-2 and pCryAB and downregulated the expression of Bax, Cyt-c, Caspase-3, and Caspase-9 expression. Additionally, Rosamultin might activate PI3K/Akt signal pathways and CryAB relative factors. Therefore, we suggest that Rosamultin could have the potential for treating H2O2-induced oxidative stress injury through its antioxidant and antiapoptosis effect.
Determination of Rosamultin in rat plasma by LC-MS/MS and its application to a pharmacokinetic study
Biomed Chromatogr 2020 Feb;34(2):e4728.PMID:31657468DOI:10.1002/bmc.4728.
A specific and reliable LC-MS/MS method for the determination of Rosamultin in rat plasma was validated. Plasma samples were prepared with protein precipitation method, and chromatographic separation was performed on a Thermo C18 analytical column (4.6 mm × 50 mm, 3.0 μm). The mass spectrometry (MS) analysis was conducted in positive SRM mode for the transitions of m/z 673.2 → 511.1 for Rosamultin and m/z 601.1 → 330.9 for IS. The method validation was conducted over the calibration range of 1.0-500 ng/mL with the precision ≤11.03% and accuracy within ±14.64%. The assay was applied to the pharmacokinetic study after oral administration of Rosamultin at a dose of 20 mg/kg in rats.
Kaji-Ichigoside F1 and Rosamultin Protect Vascular Endothelial Cells against Hypoxia-Induced Apoptosis via the PI3K/AKT or ERK1/2 Signaling Pathway
Oxid Med Cell Longev 2020 Apr 12;2020:6837982.PMID:32318240DOI:10.1155/2020/6837982.
As a pair of differential isomers, Kaji-ichigoside F1 and Rosamultin are both pentacyclic triterpenoids isolated from the subterranean root of Potentilla anserina L., a plant used in folk medicine in western China as antihypoxia and anti-inflammatory treatments. We demonstrated that Kaji-ichigoside F1 and Rosamultin effectively prevented hypoxia-induced apoptosis in vascular endothelial cells. We established a hypoxia model, using EA.hy926 cells, to further explore the mechanisms. Hypoxia promoted the phosphorylation of AKT, ERK1/2, and NF-κB. In hypoxic cells treated with Kaji-ichigoside F1, p-ERK1/2 and p-NF-κB levels were increased, while the level of p-AKT was decreased. Treatment with Rosamultin promoted phosphorylation of ERK1/2, NF-κB, and AKT in hypoxic cells. Following the addition of LY294002, the levels of p-AKT, p-ERK1/2, and p-NF-κB decreased significantly. Addition of PD98059 resulted in reduced levels of p-ERK1/2 and p-NF-κB, while p-AKT levels were increased. Pharmacodynamic analysis demonstrated that both LY294002 and PD98059 significantly inhibited the positive effects of Kaji-ichigoside F1 on cell viability during hypoxia, consistent with the results of hematoxylin-eosin (H&E) staining, DAPI staining, and flow cytometry. The antihypoxia effects of Rosamultin were remarkably inhibited by LY294002 but promoted by PD98059. In Kaji-ichigoside F1- and Rosamultin-treated cells, Bcl2 expression was significantly upregulated, while expression of Bax and cytochrome C and levels of cleaved caspase-9 and cleaved caspase-3 were reduced. Corresponding to pharmacodynamic analysis, LY294002 inhibited the regulatory effects of Kaji-ichigoside F1 and Rosamultin on the above molecules, while PD98059 inhibited the regulatory effects of Kaji-ichigoside F1 but enhanced the regulatory effects of Rosamultin. In conclusion, Kaji-ichigoside F1 protected vascular endothelial cells against hypoxia-induced apoptosis by activating the ERK1/2 signaling pathway, which positively regulated the NF-κB signaling pathway and negatively regulated the PI3K/AKT signaling pathway. Rosamultin protected vascular endothelial cells against hypoxia-induced apoptosis by activating the PI3K/AKT signaling pathway and positively regulating ERK1/2 and NF-κB signaling pathways.