| Size | Price | Stock | Qty |
|---|---|---|---|
| 100mg |
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| 250mg | |||
| Other Sizes |
| Targets |
- Target of Picroside II in sepsis model: Nuclear factor-kappa B (NF-κB) signaling pathway- Target of Picroside II in cerebral ischemia-reperfusion model: Oxidative stress-related pathways (Nrf2/HO-1, MAPK) and tight junction (TJ) protein-related signaling[2]
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|---|---|
| ln Vitro |
1. Anti-inflammatory activity in RAW264.7 macrophages (sepsis-related): RAW264.7 cells were treated with lipopolysaccharide (LPS, 1 μg/mL) and Picroside II (5 μM, 10 μM, 20 μM) for 24 hours. ELISA results showed Picroside II reduced LPS-induced secretion of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in a concentration-dependent manner: 20 μM Picroside II decreased TNF-α and IL-6 levels by ~65% and ~60%, respectively. Western blot showed Picroside II inhibited LPS-induced phosphorylation of NF-κB p65 and IκBα, and reduced nuclear translocation of p65 [1]
2. Protective effect on brain microvascular endothelial cells (BMECs) (cerebral ischemia-related): BMECs were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) and treated with Picroside II (2.5 μM, 5 μM, 10 μM). Transendothelial electrical resistance (TEER) measurement showed Picroside II reversed OGD/R-induced decrease in TEER (10 μM Picroside II restored TEER to ~85% of normal level). DCFH-DA staining showed Picroside II reduced OGD/R-induced reactive oxygen species (ROS) production (10 μM reduced ROS by ~55%). Western blot showed Picroside II upregulated OGD/R-downregulated TJ proteins (ZO-1, occludin) and Nrf2/HO-1 pathway proteins, while downregulating phosphorylated p38 MAPK [2] |
| ln Vivo |
1. Protective effect in mouse sepsis model (CLP-induced): Male C57BL/6 mice were subjected to cecal ligation and puncture (CLP) to induce sepsis, and divided into sham group, CLP model group, Picroside II 20 mg/kg group, Picroside II 40 mg/kg group. Picroside II was administered via intraperitoneal injection 1 hour before CLP and once daily for 3 days. Survival rate analysis showed Picroside II increased 7-day survival rate (40 mg/kg group: 65% vs. 20% in model group). Histopathology showed Picroside II alleviated CLP-induced lung, liver, and kidney damage (reduced inflammatory cell infiltration and tissue necrosis). ELISA showed Picroside II decreased serum TNF-α, IL-6, and IL-1β levels (40 mg/kg reduced TNF-α by ~70%), and Western blot showed reduced NF-κB activation in lung tissue [1]
2. Protective effect in rat cerebral ischemia-reperfusion model (MCAO-induced): Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2 hours followed by 24 hours of reperfusion. Rats were divided into sham group, MCAO model group, Picroside II 10 mg/kg group, Picroside II 20 mg/kg group. Picroside II was administered via tail vein injection immediately after reperfusion. Neurological deficit score showed Picroside II reduced scores (20 mg/kg group: 1.5 vs. 3.2 in model group). TTC staining showed Picroside II decreased cerebral infarction volume (20 mg/kg reduced volume by ~45%). Evans blue (EB) leakage assay showed Picroside II reduced blood-brain barrier permeability (20 mg/kg reduced EB leakage by ~50%). Biochemical analysis showed Picroside II increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) content in brain tissue [2] |
| Cell Assay |
1. RAW264.7 macrophage experiment (sepsis-related): RAW264.7 cells were seeded in 6-well plates (5×10^5 cells/well) and cultured in DMEM containing 10% fetal bovine serum. When cells reached 80% confluence, they were divided into control group, LPS group (1 μg/mL), and Picroside II groups (5 μM, 10 μM, 20 μM + 1 μg/mL LPS). After 24-hour incubation at 37°C in 5% CO2, cell supernatant was collected for ELISA (TNF-α, IL-6 detection), and cells were lysed for Western blot (p-p65, p-IκBα, nuclear p65 detection). For nuclear protein extraction, cells were treated with nuclear extraction kit, and nuclear fractions were used for Western blot [1]
2. BMEC experiment (cerebral ischemia-related): BMECs were seeded in Transwell inserts (for TEER measurement) or 6-well plates (5×10^5 cells/well) and cultured in endothelial cell medium. When cells formed a confluent monolayer, OGD was induced by replacing medium with glucose-free DMEM and incubating in 1% O2 for 4 hours; reoxygenation was performed by replacing with normal medium and incubating in 5% CO2 for 24 hours. Picroside II (2.5 μM, 5 μM, 10 μM) was added at the start of reoxygenation. TEER was measured at 0, 6, 12, 24 hours of reoxygenation. For ROS detection, cells were loaded with DCFH-DA (10 μM) for 30 minutes, and fluorescence intensity was measured by flow cytometry. For Western blot, cells were lysed to detect ZO-1, occludin, Nrf2, HO-1, and p-p38 [2] |
| Animal Protocol |
1. Mouse sepsis model (CLP) protocol: Male C57BL/6 mice (20-25 g) were anesthetized with isoflurane. A midline abdominal incision was made, cecum was ligated (70% of cecum), and punctured twice with a 22-gauge needle. Cecum was returned to abdomen, and incision was closed. Sham group only had abdominal incision without ligation/puncture. Mice were divided into 4 groups (n=15/group): sham, CLP model, Picroside II 20 mg/kg, Picroside II 40 mg/kg. Picroside II was dissolved in normal saline (0.9% NaCl) and administered via intraperitoneal injection (0.1 mL/10 g body weight) 1 hour before CLP, then once daily on days 1-3 after CLP. On day 4, mice were sacrificed; serum was collected for ELISA, and lung, liver, kidney tissues were collected for histopathology and Western blot. Survival rate was recorded for 7 days [1]
2. Rat cerebral ischemia-reperfusion model (MCAO) protocol: Male Sprague-Dawley rats (250-300 g) were anesthetized with chloral hydrate. MCAO was performed by inserting a nylon suture into the internal carotid artery to block the middle cerebral artery for 2 hours; suture was removed for 24-hour reperfusion. Sham group only had artery dissection without suture insertion. Rats were divided into 4 groups (n=8/group): sham, MCAO model, Picroside II 10 mg/kg, Picroside II 20 mg/kg. Picroside II was dissolved in normal saline and administered via tail vein injection (0.1 mL/10 g body weight) immediately after reperfusion. After 24-hour reperfusion, neurological deficit score was evaluated (0-5 scale). Rats were then sacrificed; brain was collected for TTC staining (infarction volume) and EB leakage assay (blood-brain barrier permeability). Brain tissue homogenate was prepared to detect SOD activity and MDA content [2] |
| Toxicity/Toxicokinetics |
1. In a mouse sepsis model: After 4 days of treatment with matrine II (20-40 mg/kg) via intraperitoneal injection, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine (Cr) levels were measured. No significant difference was found between the matrine II treatment group and the sham-operated group, indicating that matrine II has no hepatotoxicity or nephrotoxicity. Mice treated with matrine II had stable body weight and no significant weight loss was observed [1]
2. In a rat cerebral ischemia model: 24 hours after treatment with matrine II (10-20 mg/kg, tail vein injection), serum ALT, AST, BUN, and Cr levels were all within the normal range, and no abnormal changes in organ weight (brain, liver, kidney) were observed, indicating no acute toxicity [2] |
| References |
|
| Additional Infomation |
It has been reported that matrine II exists in Veronica anagallis, Catalpa ovata and other organisms with relevant data.
1. Matrine II is the main active ingredient isolated from the root of Scrophularia scoparia, a traditional Chinese medicine used for anti-inflammatory and hepatoprotective purposes [1][2] 2. Mechanism of sepsis: Matrine II exerts its anti-septic effect by inhibiting the NF-κB signaling pathway, reducing the production of pro-inflammatory cytokines and alleviating organ damage caused by excessive inflammation [1] 3. Mechanism of cerebral ischemia: Matrine II protects the blood-brain barrier by inhibiting oxidative stress (activating the Nrf2/HO-1 pathway and reducing ROS/MDA) and maintaining the expression of tight junction proteins, while inhibiting p38 MAPK-mediated cell damage. [2] |
| Molecular Formula |
C23H28O13
|
|---|---|
| Molecular Weight |
512.4606
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| Exact Mass |
512.153
|
| CAS # |
39012-20-9
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| PubChem CID |
11944602
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| Appearance |
White to yellow solid powder
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| Density |
1.7±0.1 g/cm3
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| Boiling Point |
780.8±60.0 °C at 760 mmHg
|
| Flash Point |
267.9±26.4 °C
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| Vapour Pressure |
0.0±2.8 mmHg at 25°C
|
| Index of Refraction |
1.681
|
| LogP |
-2.5
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| Hydrogen Bond Donor Count |
6
|
| Hydrogen Bond Acceptor Count |
13
|
| Rotatable Bond Count |
8
|
| Heavy Atom Count |
36
|
| Complexity |
839
|
| Defined Atom Stereocenter Count |
11
|
| SMILES |
COC1=C(C=CC(=C1)C(=O)O[C@H]2[C@@H]3C=CO[C@H]([C@@H]3[C@@]4([C@H]2O4)CO)O[C@H]5[C@@H]([C@H]([C@@H]([C@H](O5)CO)O)O)O)O
|
| InChi Key |
AKNILCMFRRDTEY-NUGKWEEESA-N
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| InChi Code |
InChI=1S/C23H28O13/c1-31-12-6-9(2-3-11(12)26)20(30)34-18-10-4-5-32-21(14(10)23(8-25)19(18)36-23)35-22-17(29)16(28)15(27)13(7-24)33-22/h2-6,10,13-19,21-22,24-29H,7-8H2,1H3/t10-,13-,14-,15-,16+,17-,18+,19+,21+,22+,23-/m1/s1
|
| Chemical Name |
[(1S,2S,4S,5S,6R,10S)-2-(hydroxymethyl)-10-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3,9-dioxatricyclo[4.4.0.02,4]dec-7-en-5-yl] 4-hydroxy-3-methoxybenzoate
|
| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~195.14 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.88 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (4.88 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (4.88 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.9514 mL | 9.7569 mL | 19.5137 mL | |
| 5 mM | 0.3903 mL | 1.9514 mL | 3.9027 mL | |
| 10 mM | 0.1951 mL | 0.9757 mL | 1.9514 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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