Sparstolonin B
目录号 : GC60344
An isocoumarin with diverse biological activities
Cas No.:1259330-61-4
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
Sparstolonin B is an isocoumarin that has been found in Spaganium stoloniferum and has diverse biological activities.1,2,3,4 It inhibits increases in TNF-α, IL-6, and IL-1β levels induced by the toll-like receptor 4 (TLR4) agonist LPS, TLR2 agonist Pam3CSK4 , or TLR2/6 agonist FSL-1 but not the TLR3 agonist poly(I:C) or TLR9 agonist ODN1668 in primary mouse macrophages when used at a concentration of 100 ?M.1 Sparstolonin B (1-10 ?M) reduces HIV-1 p24 antigen levels in the culture supernatant of human peripheral blood mononuclear cells (PBMCs) infected with HIV-1, indicating inhibition of HIV replication.2 It induces apoptosis, cell cycle arrest at the G2/M phase, and production of reactive oxygen species (ROS) in SH-SY5Y neuroblastoma cells when used at a concentration of 10 ?M.3 Sparstolonin B (3 and 9 mg/kg) protects mice from lethal endotoxin shock.4
1.Liang, Q., Wu, Q., Jiang, J., et al.Characterization of sparstolonin B, a chinese herb-derived compound, as a selective toll-like receptor antagonist with potent anti-inflammatory propertiesJ. Biol. Chem.286(30)26470-26479(2011) 2.Deng, X., Zhang, Y., Jiang, F., et al.The chinese herb-derived sparstolonin B suppresses HIV-1 transcriptionVirol. J.12108(2015) 3.Kumar, A., Fan, D., Dipette, D.J., et al.Sparstolonin B, a novel plant derived compound, arrests cell cycle and induces apoptosis in N-myc amplified and N-myc nonamplified neuroblastoma cellsPLoS One9(5)e96343(2014) 4.Liang, Q., Dong, S., Lei, L., et al.Protective effects of Sparstolonin B, a selective TLR2 and TLR4 antagonist, on mouse endotoxin shockCytokine75(2)302-309(2015)
| Cas No. | 1259330-61-4 | SDF | |
| Canonical SMILES | O=C1OC=C2C3=C(OC4=C2C1=C(O)C=C4)C=CC(O)=C3 | ||
| 分子式 | C15H8O5 | 分子量 | 268.22 |
| 溶解度 | DMSO : 10 mg/mL (Need ultrasonic and warming) | 储存条件 | |
| 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 | 3.7283 mL | 18.6414 mL | 37.2828 mL |
| 5 mM | 0.7457 mL | 3.7283 mL | 7.4566 mL |
| 10 mM | 0.3728 mL | 1.8641 mL | 3.7283 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。
Sparstolonin B: A Unique Anti-Inflammatory Agent
Shock 2019 Dec;52(6):568-576.PMID:30807526DOI:10.1097/SHK.0000000000001326.
Toll-like receptors are transmembrane proteins which sense and transmit infectious and inflammatory responses to the cells expressing them. Therapeutic strategies for the blockade of excessive Toll-like receptor signaling are being actively pursued for several diseases. Recently, Sparstolonin B, isolated from Chinese herb, which suppresses selectively Toll-like receptors has been studied in various inflammatory models. The objective of this review is to summarize the current literature regarding the use of Sparstolonin B in various in vitro and in vivo studies and to provide an overview regarding the potential use of this agent in different inflammatory diseases. Additionally, the current knowledge regarding the role of Toll-like receptors in inflammatory disease and the usage of various Toll-like receptor antagonists will be summarized. Based on our review, we believe Sparstolonin B could serve as a potential therapeutic agent for treatment of Toll-like receptor-mediated inflammatory disorders.
Sparstolonin B inhibits pancreatic adenocarcinoma through the NF-κB signaling pathway
Exp Cell Res 2022 Aug 1;417(1):113214.PMID:35594953DOI:10.1016/j.yexcr.2022.113214.
Pancreatic adenocarcinoma is a highly lethal malignant gastrointestinal tumor. Sparstolonin B is an isocoumarin whose anticancer activity has recently received increasing attention. This study aimed to investigate Sparstolonin B's potential antitumor effect on pancreatic adenocarcinoma. The effect of Sparstolonin B on pancreatic cancer target genes and molecular mechanism was predicted via network pharmacology; Sparstolonin B significantly decreased Panc-1 and SW1990 cell viability and effectively suppressed the proliferation, migration, and invasion of pancreatic cancer cells as shown by CCK-8, colony formation, and Transwell assays. Flow cytometry showed that it induced cell cycle arrest and apoptosis. Sparstolonin B also upregulated Bax levels but decreased those of MMP2 and Bcl-2, downregulated IκBα expression, and upregulated p65 and IκBα phosphorylation; however, it had no effect on total NF-κB p65 levels. The NF-κB pathway inhibitor QNZ reversed these effects. The treatment group (26 μmol/L) had reduced graft volume and weight and fewer Ki-67-positive cells than the control group. Therefore, Sparstolonin B can inhibit the growth and induce the apoptosis of pancreatic cancer cells via the NF-κB signaling pathway and may be a potential novel drug for pancreatic cancer treatment.
Sparstolonin B suppresses free fatty acid palmitate-induced chondrocyte inflammation and mitigates post-traumatic arthritis in obese mice
J Cell Mol Med 2022 Feb;26(3):725-735.PMID:34953038DOI:10.1111/jcmm.17099.
Abnormal lipid metabolism, such as systemic increased free fatty acid, results in overproduction of pro-inflammatory enzymes and cytokines, which is crucial in the development of obesity-related osteoarthritis (OA). However, there are only a few drugs that target the lipotoxicity of OA. Recent researches have documented that the traditional Chinese medicine, Sparstolonin B (Ssn B), exerted anti-inflammatory effects in various diseases, but not yet in OA. On the basis of this evidence, our works purposed to evaluate the effect of Ssn B on free fatty acid (FFA) palmitate (PA)-stimulated human osteoarthritic chondrocytes and obesity-associated mouse OA model. We found that Ssn B suppressed PA-triggered inflammatory response and extracellular matrix catabolism in a concentration-dependent approach. In vivo, Ssn B treatment inhibited cartilage degeneration and subchondral bone calcification caused by joint mechanical imbalance and alleviated metabolic inflammation in obesity. Mechanistically, co-immunoprecipitine and molecular docking analysis showed that the formation of toll-like receptor 4 (TLR4)/myeloid differentiation protein-2 (MD-2) complex caused by PA was blocked by Ssn B. Subsequently, it leads to inactivation of PA-caused myeloid differentiation factor 88 (MyD88)-dependent nuclear factor-kappaB (NF-κB) cascade. Together, these findings demonstrated that Ssn B is a potential treatment agent for joint degenerative diseases in obese individuals.
Sparstolonin B attenuates spinal cord injury‑induced inflammation in rats by modulating TLR4‑trafficking
Mol Med Rep 2018 Apr;17(4):6016-6022.PMID:29436632DOI:10.3892/mmr.2018.8561.
The present study used a spinal cord injury (SCI) model to evaluate whether Sparstolonin B was able to prevent SCI, and to investigate the underlying signaling mechanism. Sparstolonin B attenuated the SCI‑induced Batto, Beattie and Bresnahan score and water content in rats. Sparstolonin B attenuated the mRNA expression of proinflammatory cytokines interleukin (IL)‑18, IL‑6, IL‑1β, and IL‑23, decreased the levels of tumor necrosis factor‑α and interferon‑γ, and decreased caspase‑3 activity and apoptosis regulator Bax protein expression in SCI rats. Similarly, Sparstolonin B inhibited monocyte chemoattractant protein‑1 mRNA levels, and Toll‑like receptor (TLR) 4, myeloid differentiation primary response protein MyD88 (MyD88) and nuclear factor (NF)‑κB protein levels in SCI rats. The present results suggested that Sparstolonin B may attenuate SCI‑induced inflammation and apoptosis in rats by modulating the TLR4/MyD88/NF‑κB signaling pathway.
Anti-Inflammatory Effect of Sparstolonin B through Inhibiting Expression of NF-κB and STAT-1
Int J Mol Sci 2022 Sep 6;23(18):10213.PMID:36142124DOI:10.3390/ijms231810213.
Sparstolonin B (SsnB), which is found in Sparganium stoloniferum, prevents the synthesis of inflammatory mediators and is related to functional pathways of survival. In this study, we assessed the possible protective functions of SsnB on lipopolysaccharide (LPS)-induced inflammatory responses. We determined the functions of SsnB on controlling heme oxygenase (HO)-1, cyclooxygenase (COX-)2, and inducible nitric oxide synthase (iNOS) in LPS-activated human umbilical vein endothelial cells (HUVECs). Furthermore, the distinct function of SsnB on the expression of iNOS and well-known pro-inflammatory mediators, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, were assessed in the pulmonary histological status of LPS-injected mice. SsnB upregulated the HO-1 production, inhibited luciferase-NF-κB interaction, and lowered COX-2/PGE2 and iNOS/NO, which lead to the reduction of STAT-1 phosphorylation. Moreover, SsnB enhanced the nuclear translocation of Nrf2, elevated the binding activity between Nrf2 and antioxidant response elements (AREs), and weakened IL-1β expression on LPS-treated HUVECs. SsnB-suppressed iNOS/NO synthesis was restored by the process of the RNAi inhibition of HO-1. In experiment with an LPS-injected animal model, SsnB remarkably decreased the iNOS expression in the pulmonary biostructure and TNF-α level in the bronchoalveolar lavage fluid (BALF). Therefore, these results demonstrate that SsnB is responsible for inflammation ameliorative activity by controlling iNOS through inhibition of both NF-κB expression and p-STAT-1. Therefore, SsnB could be a candidate for promoting novel clinical substances to remedy pathologic inflammation.