Art. -Nr.: HY-W104821

Rosolic acid

Name: Rosolic acid
Brand: MedChemExpress
SKU: HY-W104821
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Rosolic acid is a Michael acceptor molecule isolated from the rhizomes of Plantago asiatica L. Rosolic acid inhibits Keap1, promotes Nrf2 nuclear translocation, and upregulates HO-1 and NQO-1. Rosolic acid reduces ER stress markers PERK, ATF-6, GRP78, and CHOP, as well as oxidative stress, ROS production, inflammation, and apoptosis. Rosolic acid upregulates SOD, CAT, and GPx activities, induces angiogenesis and insulin secretion, and restores endothelial function and pancreatic beta cell protection under ER stress. Rosolic acid can be used in research on diabetes and endothelial dysfunction.

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CAS. Nr.: 603-45-2
Formel: C₁₉H₁₄O₃
Molecular Weight:290.31

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

Data Sheet (292 KB)

Rosolic acid Chemical Structure

CAS. Nr.: 603-45-2

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Biologische Aktivität
- Beschreibung
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

Alle Glutathione Peroxidase Isoform-spezifische Produkte anzeigen :

GPX1
GPX4

In Vitro

Rosolic acid (2.5-25 μM; 24 h) does not exhibit cytotoxicity in EA.hy926 cells at concentrations up to 25 μM^[1].
Rosolic acid (15 μM; 24-48 h) is well tolerated by bovine aortic endothelial cells with no cytotoxicity up to 48 h^[3].
Rosolic acid (2.5-25 μM; 24 h) protects EA.hy926 cells against Thapsigargin (HY-13433)-induced ER stress cytotoxicity at 5 and 10 μM^[1].
Rosolic acid pretreatment (10 μM; 24 h) reduces Thapsigargin-induced ER stress markers GRP78 and CHOP in EA.hy926 cells in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) decreases GRP-78 and CHOP protein levels in EA.hy926 cells under Thapsigargin-induced ER stress in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) of EA.hy926 cells restores BCL2 expression in MIN6 pancreatic beta cells under Thapsigargin-induced ER stress in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) of EA.hy926 cells rescues PDX1 expression in MIN6 pancreatic beta cells under Thapsigargin-induced ER stress in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) of EA.hy926 cells normalizes GRP78 and CHOP expression in MIN6 pancreatic beta cells under Thapsigargin-induced ER stress in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) of EA.hy926 cells restores intracellular insulin levels in MIN6 pancreatic beta cells under Thapsigargin-induced ER stress in the co-culture setup^[1].
Rosolic acid treatment (10 μM; 24 h) upregulates Nrf2, HO-1, and NQO-1 expression in EA.hy926 cells under ER stress in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) of EA.hy926 cells upregulates Nrf2 and NQO-1 expression in MIN6 pancreatic beta cells under Thapsigargin-induced ER stress in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) of EA.hy926 cells suppresses increased MDA levels in MIN6 pancreatic beta cells under Thapsigargin-induced ER stress in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) reduces Thapsigargin-induced inflammatory cytokines and chemokines in EA.hy926 cells in the co-culture setup^[1].
Rosolic acid pretreatment (10 μM; 24 h) of EA.hy926 cells protects MIN6 pancreatic beta cells against Thapsigargin-induced reduction in viability in the co-culture setup^[1].
Rosolic acid (15 μM; 6-18 h) induces sustained HO-1 protein expression in bovine aortic endothelial cells, with continued up-regulation at 18 h^[3].
Rosolic acid (15 μM; 6 h) protects bovine aortic endothelial cells against hydrogen peroxide-induced oxidative stress^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay^[1]

Cell Line:

EA.hy926 endothelial cells
Concentration:

2.5 μM; 5 μM; 10 μM; 25 μM
Incubation Time:

24 h
Result:

Observed cytotoxicity at doses higher than 25 μM.\n
Protected cells against aThapsigargin-induced cytotoxicity at 5 and 10 μM in a dose-dependent manner.

Real Time qPCR^[1]

Cell Line:

EA.hy926 endothelial cells
Concentration:

10 μM
Incubation Time:

24 h
Result:

Significantly repressed Thapsigargin-induced GRP78 and CHOP expression to levels comparable to control.\nUpregulated Nrf2, HO-1, and NQO-1 expression.

Western Blot Analysis^[1]

Cell Line:

EA.hy926 endothelial cells
Concentration:

10 μM
Incubation Time:

24 h
Result:

Decreased GRP-78 and CHOP protein levels compared to Thapsigargin-exposed cells.

Real Time qPCR^[1]

Cell Line:

MIN6 pancreatic beta cells
Concentration:

10 μM
Incubation Time:

24 h
Result:

Restored BCL2 expression to control level.\nRescued PDX1 expression.\nUpregulated Nrf2 and NQO-1 gene expression.\nNormalized GRP78 and CHOP expression.

ELISA Assay^[1]

Cell Line:

MIN6 pancreatic beta cells
Concentration:

10 μM
Incubation Time:

24 h
Result:

Showed an intracellular insulin level comparable to control.

Cell Viability Assay^[1]

Cell Line:

MIN6 pancreatic beta cells
Concentration:

10 μM
Incubation Time:

24 h
Result:

Protected MIN6 pancreatic beta cells from Thapsigargin-induced loss of viability in a co-culture system.

Cell Viability Assay^[3]

Cell Line:

Bovine aortic endothelial cells
Concentration:

15 μM
Incubation Time:

6 h
Result:

Increased heme oxygenase activity to 2676 pmol bilirubin/mg protein/h compared to 453 pmol bilirubin/mg protein/h in control cells.
Achieved cell viability of 94% of control.

Western Blot Analysis^[3]

Cell Line:

Bovine aortic endothelial cells
Concentration:

15 μM
Incubation Time:

6 h; 18 h
Result:

Was the most potent inducer of HO-1 at 6 h among the compounds tested.
Further enhanced HO-1 expression at 18 h, whereas it was gradually decreasing with curcumin, CAPE, or 2'-hydroxychalcone.

Cell Viability Assay^[3]

Cell Line:

Bovine aortic endothelial cells
Concentration:

15 μM
Incubation Time:

24 h; 48 h
Result:

Did not produce any evident cytotoxicity at 24 or 48 h, unlike curcumin or CAPE, which caused a time-dependent decrease in cell viability.

Cell Viability Assay^[3]

Cell Line:

Bovine aortic endothelial cells
Concentration:

15 μM
Incubation Time:

6 h pretreatment; 2 h
Result:

Significantly attenuated hydrogen peroxide-mediated cytotoxicity in endothelial cells.

In Vivo

Rosolic acid (5-10 mg/kg b.w.; i.p.; once daily; 21 days) ameliorates diabetes-induced endothelial dysfunction in HFD-fed diabetic rats by activating Nrf2, reducing ER stress, inflammation, and endothelin-1 levels^[2].
Rosolic acid (1-30 mg/kg b.w.; i.p.; daily; 21 days) is safe at doses up to 10 mg/kg b.w., but doses of 30 mg/kg b.w. cause mild hepatic and renal toxicity in rats^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Wistar Albino rats (male, 100-150 g, 5-7 weeks old, high-fat diet-fed and streptozotocin-induced type-2 diabetic model)^[2]
Dosage:

5 mg/kg b.w.; 10 mg/kg b.w.
Administration:

i.p.; once daily; 21 days
Result:

Reduced cholesterol to 255.36 ± 6.83 mg/dL, triglycerides to 56.82 ± 5.63 mg/dL, VLDL to 11.38 ± 2.27 mg/dL, and LDL to 181.35 ± 11.25 mg/dL, and increased HDL to 61.28 ± 5.19 mg/dL at 10 mg/kg.
Decreased blood glucose levels starting from Day 7 at 10 mg/kg.
Improved glucose tolerance in OGTT starting from 60 minutes with peak reduction at 180 minutes.
Restored aortic tissue architecture at 5 and 10 mg/kg.
Increased NRF2 and downstream targets NQO1 and HO-1 gene expression, with a 1.8-fold increase in NRF2 protein levels at 10 mg/kg.
Dose-dependently reduced ER stress markers GRP78 and CHOP, inflammatory markers ICAM-1 and VCAM-1, and endothelin-1 expression with 5- and 2-fold reductions at 5 and 10 mg/kg, respectively.

Animal Model:

Wistar rats (female)^[2]
Dosage:

1 mg/kg b.w.; 3 mg/kg b.w.; 10 mg/kg b.w.; 30 mg/kg b.w.
Administration:

i.p.; daily; 21 days
Result:

Induced hepatic toxicity characterized by cellular damage and structural alterations in liver tissues and significant impairment of serum liver function parameters at 30 mg/kg b.w.
Induced pronounced renal cell damage including structural alterations in renal tubules and glomeruli and a significant increase in blood urea nitrogen (BUN) levels at 30 mg/kg b.w.
No toxicity or functional impairments were observed at 1, 3, and 10 mg/kg.

Chemical Information

CAS. Nr. 603-45-2
Appearance Solid
Molecular Weight 290.31
Formel C₁₉H₁₄O₃
Color White to off-white
SMILES

C1=C(C=CC(=C1)O)C(=C2C=CC(=O)C=C2)C3=CC=C(C=C3)O
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (292 KB)
SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Amin KN, et al. Effect of Rosolic acid on endothelial dysfunction under ER stress in pancreatic microenvironment. Free radical research. 2021 Jun;55(6):698-713. [Content Brief]

[2]. Amin KN, et al. Therapeutic Effect of Rosolic Acid against Endothelial Dysfunction in Diabetic Wistar Rats. Current medicinal chemistry. 2026;33(1):232-249.

[3]. Foresti R, et al. Differential activation of heme oxygenase-1 by chalcones and rosolic acid in endothelial cells. The Journal of pharmacology and experimental therapeutics. 2005 Feb;312(2):686-93.

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Rosolic acid

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