Rosmarinic acid

Synonyms: Rosemary acid

Rosmarinic acid (RA, Rosemary acid) is a naturally occurring hydroxylated compound. It has the ability to block complement fixation, inhibit lipoxygenase and cyclooxygenase activity and inhibit the expression of CCL11 and CCR3 by suppressing the IKK-β activity in NF-κB activation signaling.

Rosmarinic acid Chemical Structure

Rosmarinic acid Chemical Structure

CAS: 20283-92-5

Selleck's Rosmarinic acid has been cited by 1 publication

Purity & Quality Control

Batch: Purity: 99.88%
99.88

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Biological Activity

Description Rosmarinic acid (RA, Rosemary acid) is a naturally occurring hydroxylated compound. It has the ability to block complement fixation, inhibit lipoxygenase and cyclooxygenase activity and inhibit the expression of CCL11 and CCR3 by suppressing the IKK-β activity in NF-κB activation signaling.
Targets
IKK β [2]
(cell-based assay)
12 μM
In vitro
In vitro RA exerts a significant cytoprotective effect by scavenging intracellular ROS induced by UVB. RA also attenuates UVB-induced oxidative macromolecular damage, including protein carbonyl content, DNA strand breaks, and the level of 8-isoprostane. Furthermore, RA increases the expression and activity of superoxide dismutase, catalase, heme oxygenase-1, and their transcription factor Nrf2, which are decreased by UVB radiation. RA treatment recovers the protein expression levels of Nrf2 decreased by UVB exposure, and results in the translocation of Nrf2 protein from the cytosol into the nucleus. RA may protect cellular environments from free-radical damage and thereby, enhance the cellular antioxidant defense system[1]. Rosmarinic acid inhibits TNF-α-induced phosphorylation and degradation of IκB-α, as well as nuclear translocation of NF-κB heterodimer induced by TNF-α. It downregulates the expression of CCL11 and CCR3 via the inhibition of NF-κB activation signaling. Rosmarinic acid inhibits the Ca2+-dependent pathways of TCR-mediated signaling by inhibiting PLC-γ1 and Itk activities[2].
Cell Research Cell lines HaCaT cells
Concentrations 0.625, 1.25, 2.5, or 5 μM
Incubation Time 48 h
Method

Cells are treated with RA (0.625, 1.25, 2.5, or 5 μM) and exposed to UVB radiation 1 h later. They are then incubated at 37°C for 48 h. At this time, MTT is added to each well to obtain a total reaction volume of 200 μl. After 4 h incubation, the supernatant is removed by aspiration. The formazan crystals in each well are dissolved in dimethyl sulfoxide (DMSO; 150 μl), and the absorbance at 540 nm is measured on a scanning multi-well spectrophotometer.

In Vivo
In vivo RA improves histological and serum markers of liver damage and significantly ameliorates oxidative/nitrosative stress and inflammatory response in liver tissue. Additionally, RA prevents transforming growth factor-beta1 (TGF-b1) and alpha-smooth muscle actin (a-SMA) expression, suggesting suppression of profibrotic response. RA significantly inhibits the CCl4-induced apoptosis, which is evident from decreased cleavage of caspase-3. The hepatoprotective activity of RA coincides with enhanced NF-E2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) expression. Rosmarinic acid acts as a natural inducer of endogenous cellular antioxidant defense via activation of the Nrf2/HO-1 pathway[3].
Animal Research Animal Models Male BALB/cN mice
Dosages 10, 25 and 50 mg/kg
Administration by gavage

Chemical Information & Solubility

Molecular Weight 360.31 Formula

C18H16O8

CAS No. 20283-92-5 SDF Download Rosmarinic acid SDF
Smiles C1=CC(=C(C=C1CC(C(=O)O)OC(=O)C=CC2=CC(=C(C=C2)O)O)O)O
Storage (From the date of receipt)

In vitro
Batch:

DMSO : 72 mg/mL ( (199.82 mM); Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Water : 18 mg/mL

Ethanol : 18 mg/mL


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In vivo
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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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