Protosappanin ACAS# 102036-28-2 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 102036-28-2 | SDF | Download SDF |
| PubChem ID | 128001 | Appearance | Powder |
| Formula | C15H12O5 | M.Wt | 272.25 |
| Type of Compound | Phenols | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| SMILES | C1C(=O)COC2=C(C=CC(=C2)O)C3=CC(=C(C=C31)O)O | ||
| Standard InChIKey | MUKYVRVYBBYJSI-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C15H12O5/c16-9-1-2-11-12-6-14(19)13(18)4-8(12)3-10(17)7-20-15(11)5-9/h1-2,4-6,16,18-19H,3,7H2 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | 1. Protosappanin A exerts anti-neuroinflammatory effect by inhibiting JAK2-STAT3 pathway in lipopolysaccharide-induced BV2 microglia. 2. Protosappanin A and protosappanin B have antimicrobial activity, they show both alone activities and resistance reversal effects of amikacin and gentamicin against MRSA. 3. Protosappanin A shows strong effect against HIV-1 IN with an IC50 value of 12.6 uM. 4. Protosappanin A has anti-oxidative/nitrative activities on brain immune and neuroinflammation through regulation of CD14/TLR4-dependent IKK/IκB/NF-κB inflammation signal pathway. 5. Protosappanin A induces immunosuppression of rats heart transplantation targeting T cells in grafts via NF-kappaB pathway. |
| Targets | TNF-α | IL Receptor | JAK | STAT | ROS | NO | NADPH-oxidase | NF-kB | IkB | TLR | IFN-γ | IKK |
Protosappanin A Dilution Calculator
Protosappanin A Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.6731 mL | 18.3655 mL | 36.7309 mL | 73.4619 mL | 91.8274 mL |
| 5 mM | 0.7346 mL | 3.6731 mL | 7.3462 mL | 14.6924 mL | 18.3655 mL |
| 10 mM | 0.3673 mL | 1.8365 mL | 3.6731 mL | 7.3462 mL | 9.1827 mL |
| 50 mM | 0.0735 mL | 0.3673 mL | 0.7346 mL | 1.4692 mL | 1.8365 mL |
| 100 mM | 0.0367 mL | 0.1837 mL | 0.3673 mL | 0.7346 mL | 0.9183 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Protosappanin A induces immunosuppression of rats heart transplantation targeting T cells in grafts via NF-kappaB pathway.[Pubmed:19924402]
Naunyn Schmiedebergs Arch Pharmacol. 2010 Jan;381(1):83-92.
Protosappanin A as one major and effective ingredient from Caesalpinia sappan L. exhibited antirejection activity obviously in heart-transplanted rat. The present study was designed to screen out the potential target genes of Protosappanin A with microarray technology and reveal some molecular mechanism of immunosuppressive effect. Rats performed with ectopic peritoneal heart transplantation were randomized into three groups receiving different treatments for 7 days: Protosappanin A group (25 mg kg(-1)), cyclosporine A group (10 mg kg(-1)), and control group. The differentially expressed genes responding to Protosappanin A were analyzed with microarrays. Among common differentially expressed genes, the ones of interest were selected for further evaluation by real-time quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), Western blot, immunochemistry, immunofluorescence, and ELISA. Among the 146 common differentially expressed genes, NF-kappaB and related genes like IkappaBa, IFN-r, and IP10 were selected for verification. The results of qRT-PCR, Western blot, immunochemistry, and ELISA showed that Protosappanin A significantly reduced the expression of NF-kappaB, IFN-r, and IP10 (p < 0.05) and increased IkappaBa expression (p < 0.05) in graft. Moreover, the immunochemistry staining of NF-kappaB and IkappaBa was mainly observed in infiltrating mononuclear cells. Strikingly, immunofluorescent staining localized NF-kappaB to the TCR-positive T cells in graft. Furthermore, Protosappanin A exhibited inhibitory effect on T cell proliferation in recipients after 7-day treatment. In conclusion, Protosappanin A might act on T cells through inhibiting NF-kappaB activation and downstream gene expressions of IFN-r and IP10, meanwhile reducing T cell proliferation responding to alloantigen, so as to induce immunosuppressive effect. The results encourage a potential therapeutic evaluation of Protosappanin A for clinical organ transplantation or other T cell-mediated immune disorders. Additionally, our study also verified the feasibility of microarray utilization in Chinese herb research to explore molecular mechanism and promote development of scientific theories.
Protosappanin A inhibits oxidative and nitrative stress via interfering the interaction of transmembrane protein CD14 with Toll-like receptor-4 in lipopolysaccharide-induced BV-2 microglia.[Pubmed:23000519]
Int Immunopharmacol. 2012 Dec;14(4):558-69.
Oxidative and nitrative stresses have been established to play a pivotal role in neuroinflammation. During inflammation-mediated neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, reactive oxygen species (ROS) and nitric oxide (NO) are produced by activated microglia, further inducing increased neuronal injury in the brain. Protosappanin A (PTA) is a bioactive compound isolated from a traditional Chinese medicine, Caesalpinia sappan L. (Lignum Sappan), showing immunosuppressive effects. However, the molecular mechanisms responsible for the anti-oxidative and nitrative activity of PTA have not been elucidated, particularly in central nervous system. In this study, we found that PTA significantly inhibited ROS and NO production by suppression of NADPH oxidase and inducible nitric oxide synthase (iNOS) activity on lipopolysaccharide (LPS)-stimulated BV-2 microglia. Moreover, PTA modulated IKK/IkappaB/NF-kappaB inflammation signal pathway to inhibit the activity and expressions of NADPH oxidase and iNOS. A further study indicated that PTA didn't inhibit LPS interaction with transmembrane protein CD14, which is a receptor for LPS binding. However, PTA interfered with the interaction of CD14 with Toll-like receptor (TLR4), an early cell event of IKK/IkappaB/NF-kappaB inflammation signal activation, resulting in a block on LPS translocation from CD14 to TLR4. Therefore, CD14/TLR4 interaction may be a potential drug target in neuroinflammation-related oxidative and nitrative stress. Taken together, these results suggest that PTA has anti-oxidative/nitrative activities on brain immune and neuroinflammation through regulation of CD14/TLR4-dependent IKK/IkappaB/NF-kappaB inflammation signal pathway.
Antimicrobial activity and synergy of antibiotics with two biphenyl compounds, protosappanins A and B from Sappan Lignum against methicillin-resistant Staphylococcus aureus strains.[Pubmed:25920539]
J Pharm Pharmacol. 2015 Oct;67(10):1439-47.
OBJECTIVES: This study aims to investigate antimicrobial ingredients from Sappan Lignum and to evaluate their synergy on methicillin-resistant Staphylococcus aureus strains with antibiotics. METHODS: Bioactivity-guided phytochemical procedures were used to screen the active compounds. Minimum inhibitory concentrations (MICs) and minimum bactericidal concentrations (MBCs) were assayed by broth microdilution. The synergy was evaluated through checkerboard microdilution and loss of viability assays. KEY FINDINGS: Protosappanins A (PsA) and B (PsB) were identified from Sappan Lignum extracts. They showed active against both S. aureus and MRSA with MIC or MIC50 at 64 (PsA) and 128 (PsB) mg/L alone. When they were used in combination with antibiotics, they showed best synergy with amikacin and gentamicin with MIC50 (mg/L) of amikacin reduced more significantly from 32 to four (with PsA) and eight (with PsB), and the fractional inhibitory concentration index (FICI) ranged between 0.078 and 0.500 (FICI50 = 0.375). Moreover, the resistance of MRSA towards amikacin and gentamicin could be reversed by the Clinical and Laboratory Standards Institute criteria. The combined bactericidal mode could as well be synergy. PsA and PsB showed very low cytotoxicity in comparison with their promising activity against MRSA. CONCLUSIONS: Protosappanins A and B showed both alone activities and resistance reversal effects of amikacin and gentamicin against MRSA, which warrant further investigations for potential combinatory therapy of MRSA infection.
Protosappanin A exerts anti-neuroinflammatory effect by inhibiting JAK2-STAT3 pathway in lipopolysaccharide-induced BV2 microglia.[Pubmed:28991528]
Chin J Nat Med. 2017 Sep;15(9):674-679.
Microglial activation and resultant neuroinflammatory response are implicated in various brain diseases including Alzheimer's disease and Parkinson's disease. Treatment with anti-neuroinflammatory agents could provide therapeutic benefits for such disorders. Protosappanin A (PTA) is a major bioactive ingredient isolated from Caesalpinia sappan L.. In this work, the anti-neuroinflammatory effects of PTA on LPS-stimulated BV2 cells were investigated and the underlying mechanisms were explored. Results showed that PTA significantly inhibited the production of TNF-alpha and IL-1beta in LPS-activated BV2 microglia. Moreover, the mRNA expressions of IL-6, IL-1beta, and MCP-1 were reduced by PTA in a dose-dependent manner. Furthermore, PTA suppressed JAK2/STAT3-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3, as well as STAT3 nuclear translocation against LPS treatment. These observations suggested a novel role for PTA in regulating LPS-induced neuroinflammatory injuries.
