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Isoastragaloside I is a natural compound found in Astragalus membranaceus, with oral activity and multiple biological activities such as anti-inflammatory and antioxidant properties. Isoastragaloside I inhibits Akt, NF-κB, MAPKs and PI3K, enhances the activity of hepatic FXR, regulates the TGF-β/Smads signaling pathway, and upregulates antioxidant molecules downstream of Nrf2. Isoastragaloside I inhibits the expression of NO, TNF-α, iNOS, COX-2, IL-1β and VCAM-1, and reduces intracellular ROS levels. Isoastragaloside I attenuates blood-brain barrier disruption, restores intestinal barrier function, increases β-cell mass, improves glucose homeostasis, and elevates circulating adiponectin levels. Isoastragaloside I can be used for the study of neuroinflammation-related neurodegenerative diseases, cholestatic liver disease, and diabetes.
For research use only. We do not sell to patients.
Isoastragaloside I is a natural compound found in Astragalus membranaceus, with oral activity and multiple biological activities such as anti-inflammatory and antioxidant properties. Isoastragaloside I inhibits Akt, NF-κB, MAPKs and PI3K, enhances the activity of hepatic FXR, regulates the TGF-β/Smads signaling pathway, and upregulates antioxidant molecules downstream of Nrf2. Isoastragaloside I inhibits the expression of NO, TNF-α, iNOS, COX-2, IL-1β and VCAM-1, and reduces intracellular ROS levels. Isoastragaloside I attenuates blood-brain barrier disruption, restores intestinal barrier function, increases β-cell mass, improves glucose homeostasis, and elevates circulating adiponectin levels. Isoastragaloside I can be used for the study of neuroinflammation-related neurodegenerative diseases, cholestatic liver disease, and diabetes[1][2][3][4].
Isoastragaloside I (ISO I) (25-100 μM; 24 h) has no cytotoxic effect on BV-2 microglial cells[1]. Isoastragaloside I (25-100 μM; 2 h pre-treatment, followed by 20 h LPS stimulation) dose-dependently inhibits LPS-induced nitric oxide and TNF-α secretion from BV-2 microglial cells[1]. Isoastragaloside I (100 μM; 2 h pre-treatment, followed by 20 h LPS stimulation) inhibits LPS-induced expression of iNOS and COX-2 proteins in BV-2 microglia and phosphorylation of NF-κB, IκBα, p38, JNK and ERK1/2[1]. Isoastragaloside I (100 μM; 2 h pre-treatment, followed by 20 h LPS stimulation) downregulates LPS-induced TNF-α, IL-1β, and iNOSmRNA expression in BV-2 microglial cells[1]. Isoastragaloside I (100 μM; 2 h pre-treatment, followed by 20 h LPS stimulation) inhibits LPS-induced transactivation of NF-κB in BV-2 microglia. It blocked LPS-induced nuclear translocation of phosphorylated NF-κB in BV-2 microglia[1]. Isoastragaloside I (100 μM; 2 h pre-treatment, followed by 5-30 min LPS stimulation) suppresses LPS-induced phosphorylation of PI3K and Akt in BV-2 microglial cells[1]. Isoastragaloside I (ISOI) (25-100 μM; 2 h pre-incubation, 1-24 h co-treatment with LPS) pre-treatment prevents LPS-induced TEER reduction in bEnd.3 cells[3]. Isoastragaloside I (25-100 μM; 2 h pre-incubation, 24 h co-treatment with LPS) pre-treatment mitigates LPS-induced Na+F− exudation in bEnd.3 cells, reduced ROS accumulation, and restored the expression of tight junction proteins (ZO-1, occludin, claudin-5)[3]. Isoastragaloside I (25-100 μM; 2 h pre-incubation, 24 h co-treatment with LPS) pre-treatment reduces LPS-induced JAWS II monocyte adhesion to bEnd.3 cells[3]. Isoastragaloside I pre-treatment reduces LPS-induced mRNA expression of IL-1β, TNF-α, VCAM-1, and ICAM-1 in bEnd.3 cells[3]. Isoastragaloside I (100 μM; 2 h pre-incubation, 24 h co-treatment with LPS) pre-treatment suppresses LPS-induced VCAM-1 protein expression in bEnd.3 cells and restored LPS-depleted Nrf2, HO-1, and NQO1 protein expression in bEnd.3 cells[3]. Isoastragaloside I (25-100 μM; 24 h) activates Nrf2 transactivation in HEK293T cells[3]. Isoastragaloside I (100 μM; 2 h pre-incubation, 24 h co-treatment with LPS) pre-treatment enhances LPS-reduced Nrf2 nuclear translocation in bEnd.3 cells[3]. Isoastragaloside I (100 μM; 2 h pre-incubation, 12 or 24 h co-treatment with LPS after Nrf2 siRNA transfection) pre-treatment's ability to restore the expression of tight junction proteins and VCAM-1 in LPS-stimulated bEnd.3 cells, which depends on the Nrf2 signaling pathway, as silencing Nrf2 eliminates this effect[3]. Isoastragaloside I (10 μM) inhibits pancreatic ductal organoid growth in vitro, while low doses do not alter organoid cell proliferation[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
2 h pre-treatment, followed by 20 h LPS stimulation
Result:
Reduced LPS-triggered iNOS and COX-2 protein expression, and suppressed the phosphorylation of NF-κB and IκBα. Mitigated LPS-induced activation of p38, JNK and ERK1/2.
Rescued LPS-induced reductions of ZO-1, occludin, and claudin-5 protein expression, with significant restoration of occludin and claudin-5 levels, and visible restoration of ZO-1 membrane localization. Restrained LPS-induced elevation of VCAM-1 protein levels and restored LPS-mediated downregulation of Nrf2, HO-1 and NQO1 protein expression.
2 h pre-incubation; 12 or 24 h co-treatment with LPS, after Nrf2 siRNA transfection
Result:
No longer exerted a significant effect on ZO-1, occludin, or claudin-5 levels when Nrf2 was silenced.\nDid not reverse LPS-induced VCAM-1 expression elevation when Nrf2 was silenced.
In Vivo
Isoastragaloside I (IAS I) (20-50 mg/kg; p.o.; daily; 4 weeks) dose-dependently alleviates DDC-induced cholestatic liver disease in C57BL/6J mice, with significant improvements in liver injury, fibrosis, inflammation, bile acid metabolism and intestinal barrier function[2]. Isoastragaloside I (IAS-I) (0.5-5 mg/kg; intravenous injection; days 0-21) significantly increases the mass of small islets by approximately 60% in healthy mice; it also alleviates symptoms and increases small islet mass in both type 1 and type 2 diabetic mice[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Increased body weight dose-dependently compared to the DDC model group. Reduced liver weight and liver/body weight ratio significantly. Reduced intraluminal porphyrin embolism, inflammatory cell aggregation, and portal duct reaction via H&E staining. Reduced collagen deposition significantly via Sirius Red staining. Dose-dependently reduced levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin, direct bilirubin, alkaline phosphatase, and total bile acid compared to the DDC model group. Reduced liver hydroxyproline content and Sirius Red-positive area significantly. Reduced positive areas and mRNA/protein expression of cholangiocyte biomarkers cytokeratin 19 and cytokeratin 7 significantly. Reduced positive area and mRNA/protein expression of α-smooth muscle actin significantly. Reduced mRNA expression of collagen type I alpha 1 chain, collagen type IV, and transforming growth factor-β1 significantly. Reduced protein expression of TGF-β1 and phosphorylated Smad2/3 (p-Smad2/3)/Smad2/3 significantly. Reduced positive area and mRNA expression of F4/80 significantly. Reduced mRNA expression of tumor necrosis factor-α and interleukin-1β significantly. Reduced protein expression of interleukin-6 and CD68 significantly. Reduced levels of arachidonic acid metabolites 5-hydroxyeicosatetraenoic acid, 15-HETE, 11(S)-HETE, prostaglandin E2, prostaglandin D2, 14(15)-DiHET, and 11(12)-DiHET significantly. Increased levels of ω-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid significantly. Increased fecal bile acid concentrations, including tau-BAs, gly-BAs, uncon-BAs, and total BAs significantly. Normalized serum and liver bile acid profiles, with significant reductions in total BAs, uncon-BAs, con-BAs, and tau-BAs compared to the DDC model group. Increased liver levels of taurocholic acid, taurohyocholic acid, taurodeoxycholic acid, and taurochenodeoxycholic acid significantly. Increased mRNA expression of hepatic farnesoid X receptor, small heterodimer partner, cholesterol 7α-hydroxylase, sodium taurocholate cotransport peptide, and bile-salt export pump significantly. Increased protein expression of FXR and Cyp7a1 significantly. Improved colonic mucosal structural integrity, reduced inflammatory cell infiltration, and restored goblet cell count. Increased positive area and mRNA expression of zonula occludens protein 1 significantly. Increased mRNA expression of Occludin and Muc2 significantly. Increased protein expression of Occludin significantly.
Induced a statistically significant ~60% increase in small islet mass compared to controls at 0.5 mg/kg. Showed a non-significant trend towards increased total β-cell proportion and total β-cell mass at both doses.
Animal Model:
C57BL/6 (6-week-old, type 2 diabetes induced by 3 months high-fat diet + 3 consecutive daily i.p. 50 mg/kg streptozotocin, blood glucose >16.7 mM on two consecutive days)[4]
Dosage:
0.5 mg/kg; 5 mg/kg
Administration:
i.v.; days 0, 3, 7, 10, 14, 17, 21
Result:
Alleviated hyperglycaemia at both doses without affecting body weight. Improved insulin resistance only at 0.5 mg/kg (~40% AUC reduction), but not at 5 mg/kg, and did not improve glucose responsiveness at either dose. Increased small islet mass at both doses, with a non-significant trend towards increased total β-cell mass.
Animal Model:
ICR (8-week-old, type 1 diabetes induced by single i.p. 150 mg/kg Streptozotocin (HY-13753), blood glucose >16.7 mM on two consecutive days)[4]
Dosage:
0.5 mg/kg
Administration:
i.v.; days 0, 3, 7, 10, 14, 17, 21
Result:
Reduced fasting blood glucose without affecting body weight or glucose responsiveness. Increased β-cell proportion and total β-cell mass in the pancreas, as well as β-cell proportion in both small and large islets. Found that proliferating β-cells accounted for only 0.009% of total pancreatic cells, indicating the increase in β-cell mass was not primarily mediated by β-cell proliferation.
Animal Model:
SOX9-CreERT2; R26-LSL-tdTomato (type 1 diabetes induced by single i.p. 150 mg/kg streptozotocin, blood glucose >16.7 mM on two consecutive days; ductal cells labelled via 5 consecutive daily i.p. 75 mg/kg tamoxifen (HY-13757A) prior to diabetes induction)[4]
Dosage:
0.5 mg/kg
Administration:
i.v.; days 0, 3, 7, 10, 14, 17, 21
Result:
Alleviated hyperglycaemia compared to controls. Showed co-localization of tdTomato+ duct-derived cells with Insulin+ β-cells in islets and small islets, and significantly increased the proportion of duct-derived Insulin+ cells to 3.1% of total tdTomato+ cells compared to controls. Resulted in proliferating β-cells almost exclusively arising from SOX9-derived cells.
DMSO : 50 mg/mL (57.53 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
1.1507 mL
5.7535 mL
11.5070 mL
5 mM
0.2301 mL
1.1507 mL
2.3014 mL
10 mM
0.1151 mL
0.5753 mL
1.1507 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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