Rosmarinic acid

Anti-inflammatory, cytostatic and antiviral; GPR35 agonist CAS# 20283-92-5

Rosmarinic acid

Catalog No. BCN5893----Order now to get a substantial discount!

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Quality Control of Rosmarinic acid

Number of papers citing our products

Chemical structure

Rosmarinic acid

3D structure

Chemical Properties of Rosmarinic acid

Cas No. 20283-92-5 SDF Download SDF
PubChem ID 5281792 Appearance White-beige powder
Formula C18H16O8 M.Wt 360.31
Type of Compound Phenylpropanoids Storage Desiccate at -20°C
Synonyms Labiatenic acid
Solubility DMSO : 100 mg/mL (277.54 mM; Need ultrasonic)
Chemical Name (2R)-3-(3,4-dihydroxyphenyl)-2-[(E)-3-(3,4-dihydroxyphenyl)prop-2-enoyl]oxypropanoic acid
SMILES C1=CC(=C(C=C1CC(C(=O)O)OC(=O)C=CC2=CC(=C(C=C2)O)O)O)O
Standard InChIKey DOUMFZQKYFQNTF-WUTVXBCWSA-N
Standard InChI InChI=1S/C18H16O8/c19-12-4-1-10(7-14(12)21)3-6-17(23)26-16(18(24)25)9-11-2-5-13(20)15(22)8-11/h1-8,16,19-22H,9H2,(H,24,25)/b6-3+/t16-/m1/s1
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.
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.
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.

Source of Rosmarinic acid

1 Anchusa sp. 2 Astrantia sp. 3 Collinsonia sp. 4 Eryngium sp. 5 Glechoma sp. 6 Heliotropium sp. 7 Hyssopus sp. 8 Lavandula sp. 9 Lithospermum sp. 10 Lycopus sp. 11 Malva sp. 12 Melissa sp. 13 Mentha sp. 14 Nepeta sp. 15 Origanum sp. 16 Orthosiphon sp. 17 Perilla sp. 18 Pulmonaria sp. 19 Rosmarinus sp. 20 Salvia sp. 21 Sanicula sp. 22 Satureja sp. 23 Thymus sp.

Biological Activity of Rosmarinic acid

DescriptionRosmarinic acid has antiviral, antibacterial, antiinflammatory, neuroprotective, anticancer, anti-lipid peroxidative, apoptotic,and antioxidant activities. It is used for food preservation, and to treat peptic ulcers, arthritis, cataract, cancer, rheumatoid arthritis, bronchial asthma, and several human neurodegenerative diseases caused by oxidative stress. Rosmarinic acid 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. It inhibits MAO-A, MAO-B and COMT enzymes with IC50s of 50.1, 184.6 and 26.7 μM, respectively.
TargetsTNF-α | IL Receptor | NO | JNK | p38MAPK | NF-kB | ROS | PI3K | MAO-A | MAO-B | COMT | IKK
In vitro

Epigallocatechin gallate, ellagic acid, and rosmarinic acid perturb dNTP pools and inhibit de novo DNA synthesis and proliferation of human HL-60 promyelocytic leukemia cells: Synergism with arabinofuranosylcytosine.[Pubmed: 25636891]

Phytomedicine. 2015 Jan 15;22(1):213-22.

Epigallocatechin gallate (EGCG), ellagic acid (EA) and Rosmarinic acid (RA) are natural polyphenols exerting cancer chemopreventive effects. Ribonucleotide reductase (RR; EC 1.17.4.1) converts ribonucleoside diphosphates into deoxyribonucleoside diphosphates being essential for DNA replication, which is why the enzyme is considered an excellent target for anticancer therapy.
METHODS AND RESULTS:
EGCG, EA, and RA dose-dependently inhibited the growth of human HL-60 promyelocytic leukemia cells, exerted strong free radical scavenging potential, and significantly imbalanced nuclear deoxyribonucleoside triphosphate (dNTP) concentrations without distinctly affecting the protein levels of RR subunits (R1, R2, p53R2). Incorporation of (14)C-cytidine into nascent DNA of tumor cells was also significantly lowered, being equivalent to an inhibition of DNA synthesis. Consequently, treatment with EGCG and RA attenuated cells in the G0/G1 phase of the cell cycle, finally resulting in a pronounced induction of apoptosis. Sequential combination of EA and RA with the first-line antileukemic agent arabinofuranosylcytosine (AraC) synergistically potentiated the antiproliferative effect of AraC, whereas EGCG plus AraC yielded additive effects.
CONCLUSIONS:
Taken together, we show for the first time that EGCG, EA, and RA perturbed dNTP levels and inhibited cell proliferation in human HL-60 promyelocytic leukemia cells, with EGCG and RA causing a pronounced induction of apoptosis. Due to these effects and synergism with AraC, these food ingredients deserve further preclinical and in vivo testing as inhibitors of leukemic cell proliferation.

Rosmarinic acid mediated neuroprotective effects against H2O2-induced neuronal cell damage in N2A cells.[Pubmed: 25058919 ]

Life Sci. 2014 Sep 15;113(1-2):7-13.

Oxidative stress plays a key role in several ailments including neurodegenerative conditions. The aim of the study was to demonstrate the effect of Rosmarinic acid (RA) in preventing oxidative stress related death of neuronal cell lines.
METHODS AND RESULTS:
In the present study, we demonstrated direct neuroprotective effect of RA using H2O2-induced oxidative challenge in N2A mouse neuroblastoma cells. The mechanism of neutralization of H2O2-induced toxicity by RA was evaluated using MTT, lactate dehydrogenase, mitochondrial membrane potential (MMP), intracellular ROS, and comet assays. Up-regulation of brain neuronal markers at molecular level was performed by RT-PCR. Results presented in the paper indicate that H2O2-induced cytotoxicity in N2A cells was suppressed by treatment with RA. Moreover, RA is very effective in attenuating the disruption of lactate dehydrogenase, mitochondrial membrane potential and intracellular ROS. Pretreatment with RA significantly prevents genotoxicity (3.7-fold, p<0.01) and promotes the up-regulation of tyrosine hydroxylase (TH) (4.5-fold, p<0.01), and brain-derived neurotrophic factor (BDNF) genes (5.4-fold, p<0.01) against H2O2-induced cytotoxicity in N2A cells.
CONCLUSIONS:
Our results revealed that N2A cells are suitable cellular models to evaluate neuroprotective effects of RA, and suggest that RA may potentially serve as an agent for prevention of several human neurodegenerative diseases caused by oxidative stress.

Rosmarinic acid induces melanogenesis through protein kinase A activation signaling.[Pubmed: 17651699 ]

Biochem Pharmacol. 2007 Oct 1;74(7):960-8.

Melanogenesis is a physiological process that results in the synthesis of melanin pigments, which play a crucial protective role against skin photocarcinogenesis.
METHODS AND RESULTS:
In order to determine the effects of Rosmarinic acid on melanogenesis and elucidate the molecular events of melanogenesis induced by Rosmarinic acid, several experiments were performed in B16 melanoma cells. In this study, we showed that the melanin content and tyrosinase expression were increased by Rosmarinic acid in a concentration-dependent manner. In addition, after the melanin content was increased by Rosmarinic acid, it was reduced by H-89 and KT 5720, protein kinase A (PKA) inhibitors, but not by SB203580, a p38(mapk) inhibitor, or Ro-32-0432, a PKC inhibitor, which suggests the involvement of PKA in Rosmarinic acid-induced melanogenesis. Consistent with this, Rosmarinic acid induced the phosphorylation of CRE-binding protein (CREB), but had no effect on the phosphorylation of p38(mapk) or the inhibition of Akt phosphorylation. Additionally, Rosmarinic acid induced the activation of cAMP response element (CRE) without having any effect on cAMP production, which suggests that Rosmarinic acid-induced melanogenesis is mediated by PKA, which occurs downstream of cAMP production. This result was further confirmed by the fact that Rosmarinic acid-induced phosphorylation of CREB was inhibited by H-89, but not by PD98059, a MEK1 inhibitor, or by LY294002, a phosphatidylinositol-3-kinase (PI3K) inhibitor. Rosmarinic acid-induced expression of tyrosinase protein was attenuated by H-89.
CONCLUSIONS:
Based on these results, we report for the first time that Rosmarinic acid induces melanogenesis through PKA activation signaling.

Rosmarinic acid as a downstream inhibitor of IKK-beta in TNF-alpha-induced upregulation of CCL11 and CCR3.[Pubmed: 16604092 ]

Br J Pharmacol. 2006 Jun;148(3):366-75.

1. Tumor necrosis factor (TNF)-alpha is known to induce the expression of CCL11 and CCR3 via the activation of NF-kappaB. CCL11 (eotaxin), the C-C chemokine, is a potent chemoattractant for eosinophils and Th2 lymphocytes, and CCR3 is the receptor for CCL11.
METHODS AND RESULTS:
2. In order to determine the effects of Rosmarinic acid on the TNF-alpha-induced upregulation of CCL11 and CCR3 in human dermal fibroblasts, we performed an enzyme-linked immunosorbent assay for CCL11 and a Western blot assay for CCR3. The TNF-alpha-induced expression of CCL11 and CCR3 genes was attenuated by Rosmarinic acid. 3. In our NF-kappaB luciferase reporter system, TNF-alpha-induced NF-kappaB activation was observed to be reduced by Rosmarinic acid. In accordance with this result, Rosmarinic acid also inhibited TNF-alpha-induced phosphorylation and degradation of IkappaB-alpha, as well as nuclear translocation of NF-kappaB heterodimer induced by TNF-alpha. This suggests that Rosmarinic acid downregulates the expression of CCL11 and CCR3 via the inhibition of NF-kappaB activation signaling. 4. Using the NF-kappaB luciferase reporter system, Western blot analysis, and IKK-beta activity assay, we determined that Rosmarinic acid inhibits IKK-beta activity in NF-kappaB signaling, which upregulates the expression of CCL11 and CCR3. Additionally, TNF-alpha-induced secretion of soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 molecules was found to be attenuated by Rosmarinic acid.
CONCLUSIONS:
5. Our results show that Rosmarinic acid inhibits the expression of CCL11 and CCR3 by suppressing the IKK-beta activity in NF-kappaB activation signaling. Further, these results suggest that Rosmarinic acid might inhibit the expression of NF-kappaB promoter-related genes.

In vivo

Rosmarinic acid modulates the antioxidant status and protects pancreatic tissues from glucolipotoxicity mediated oxidative stress in high-fat diet: streptozotocin-induced diabetic rats.[Pubmed: 25735949]

Mol Cell Biochem. 2015 Mar 4.

Persistent hyperglycemia and elevated levels of free fatty acids (FFA) contribute to oxidative stress, a proximate cause for the onset and progression of diabetes and its complications.
METHODS AND RESULTS:
The present study was hypothesized to evaluate the anti-diabetic potential of Rosmarinic acid (RA) during high-fat diet (HFD)-streptozotocin (STZ)-induced type 2 Diabetes (T2D) in wistar albino rats. Oral administration of RA (100 mg/kg b.w) significantly (p < 0.05) increased the insulin sensitivity index (ISI0,120), while the levels of blood glucose, HbA1c, advanced glycation end products (AGE), TNF-α, IL-1β, IL 6, NO, p-JNK, P38 MAPK and NF-κB were significantly reduced, with a concomitant elevation in the plasma insulin levels in diabetic rats. Furthermore, RA treatment significantly (p < 0.05) reduced the levels of triglycerides, FFA and cholesterol in serum, and reduced the levels of lipid peroxides, AOPP's and protein carbonyls in the plasma and pancreas of diabetic rats. The diminished activities of pancreatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) and the decreased levels of plasma ceruloplasmin, vitamin C, vitamin E and reduced glutathione (GSH) in diabetic rats were also significantly (p < 0.05) recovered upon RA treatment denoting its antioxidant potential which was confirmed by Nrf-2, hemeoxyenase (HO-1) levels. Histological, ultrastructural and immunohistochemical data demonstrate that oral administration of RA protects pancreatic β-cells from oxidative niche in HFD-STZ-induced experimental diabetes.
CONCLUSIONS:
Our findings suggest that the oral treatment with RA alleviates pancreatic β-cell dysfunction and glucolipotoxicity-mediated oxidative stress during HFD-STZ-induced T2DM, perhaps through its antioxidant potential.

Protocol of Rosmarinic acid

Cell Research

Rosmarinic Acid Attenuates Cell Damage against UVB Radiation-Induced Oxidative Stress via Enhancing Antioxidant Effects in Human HaCaT Cells.[Pubmed: 26759705 ]

Biomol Ther (Seoul). 2016 Jan;24(1):75-84.

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.

Animal Research

Antiepileptogenic, antioxidant and genotoxic evaluation of rosmarinic acid and its metabolite caffeic acid in mice.[Pubmed: 25498895]

Life Sci. 2015 Feb 1;122:65-71.

Animal Models: Male CF-1 mice
Formulation: ---
Dosages:1, 2 or 4mg/kg, once every three days during 16days
Administration: i.p.

Rosmarinic acid Dilution Calculator

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Rosmarinic acid Molarity Calculator

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Preparing Stock Solutions of Rosmarinic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.7754 mL 13.8769 mL 27.7539 mL 55.5078 mL 69.3847 mL
5 mM 0.5551 mL 2.7754 mL 5.5508 mL 11.1016 mL 13.8769 mL
10 mM 0.2775 mL 1.3877 mL 2.7754 mL 5.5508 mL 6.9385 mL
50 mM 0.0555 mL 0.2775 mL 0.5551 mL 1.1102 mL 1.3877 mL
100 mM 0.0278 mL 0.1388 mL 0.2775 mL 0.5551 mL 0.6938 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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Background on Rosmarinic acid

Rosmarinic acid (RA) is a widespread phenolic ester compound in the plants. Rosmarinic acid inhibits MAO-A, MAO-B and COMT enzymes with IC50s of 50.1, 184.6 and 26.7 μM, respectively.

In Vitro:Rosmarinic acid (RA) shows an in vitro multifunctional profile characterized by antioxidant effects, and monoamine oxidases (MAO-A and MAO-B) and catechol-O-methyl transferase (COMT) inhibition. Rosmarinic acid shows antioxidant effects against hydroxyl (HO(•)) and nitric oxide (NO) radicals (IC50 of 29.4 and 140 μM, respectively), and inhibition of lipid peroxidation (IC50 of 19.6 μM)[1]. Rosmarinic acid (RA) exerts a significant cytoprotective effect by scavenging intracellular ROS induced by UVB. In H2O2-treated cells, 2.5 μM Rosmarinic acid scavenges 60% of intracellular ROS compared to 77% of intracellular ROS scavenging effect in N-acetyl-L-cysteine (NAC)[2].

In Vivo:Rosmarinic acid (RA) is a widespread phenolic ester compound in the plants, particularly those in the Labiatae family of herbs, such as Rosmarinus officinali, Salvia miltiorrhiza, and Prunella vulgaris. Rosmarinic acid suppresses colonic inflammation in dextran sulphate sodium (DSS)-induced mice via dual inhibition of NF-κB and STAT3 activation. In the DSS-induced colitis model, Treatment with Rosmarinic acid (30, 60 mg/kg, p.o.) markedly attenuates the production of cytokines[3].

References:
[1]. Andrade JM, et al. Combining in vitro and in silico approaches to evaluate the multifunctional profile of rosmarinic acid from Blechnum brasiliense on targets related to neurodegeneration. Chem Biol Interact. 2016 Jul 25;254:135-45. [2]. Fernando PM, et al. Rosmarinic Acid Attenuates Cell Damage against UVB Radiation-Induced Oxidative Stress via Enhancing Antioxidant Effects in Human HaCaT Cells. Biomol Ther (Seoul). 2016 Jan;24(1):75-84. [3]. Jin BR, et al. Rosmarinic acid suppresses colonic inflammation in dextran sulphate sodium (DSS)-induced mice via dual inhibition of NF-κB and STAT3 activation. Sci Rep. 2017 Apr 6;7:46252.

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References on Rosmarinic acid

Epigallocatechin gallate, ellagic acid, and rosmarinic acid perturb dNTP pools and inhibit de novo DNA synthesis and proliferation of human HL-60 promyelocytic leukemia cells: Synergism with arabinofuranosylcytosine.[Pubmed:25636891]

Phytomedicine. 2015 Jan 15;22(1):213-22.

Epigallocatechin gallate (EGCG), ellagic acid (EA) and Rosmarinic acid (RA) are natural polyphenols exerting cancer chemopreventive effects. Ribonucleotide reductase (RR; EC 1.17.4.1) converts ribonucleoside diphosphates into deoxyribonucleoside diphosphates being essential for DNA replication, which is why the enzyme is considered an excellent target for anticancer therapy. EGCG, EA, and RA dose-dependently inhibited the growth of human HL-60 promyelocytic leukemia cells, exerted strong free radical scavenging potential, and significantly imbalanced nuclear deoxyribonucleoside triphosphate (dNTP) concentrations without distinctly affecting the protein levels of RR subunits (R1, R2, p53R2). Incorporation of (14)C-cytidine into nascent DNA of tumor cells was also significantly lowered, being equivalent to an inhibition of DNA synthesis. Consequently, treatment with EGCG and RA attenuated cells in the G0/G1 phase of the cell cycle, finally resulting in a pronounced induction of apoptosis. Sequential combination of EA and RA with the first-line antileukemic agent arabinofuranosylcytosine (AraC) synergistically potentiated the antiproliferative effect of AraC, whereas EGCG plus AraC yielded additive effects. Taken together, we show for the first time that EGCG, EA, and RA perturbed dNTP levels and inhibited cell proliferation in human HL-60 promyelocytic leukemia cells, with EGCG and RA causing a pronounced induction of apoptosis. Due to these effects and synergism with AraC, these food ingredients deserve further preclinical and in vivo testing as inhibitors of leukemic cell proliferation.

Antiallergic activity of rosmarinic acid esters is modulated by hydrophobicity, and bulkiness of alkyl side chain.[Pubmed:25686361]

Biosci Biotechnol Biochem. 2015;79(7):1178-82.

Methyl, propyl and hexyl esters of rosmarinic, caffeic and p-coumaric acids were tested for antiallergic activity, and Rosmarinic acid propyl ester exhibited the greatest beta-hexosaminidase release suppression (IC50, 23.7 muM). Quadratic correlations between pIC50 and cLogP (r(2) = 0.94, 0.98, and 1.00, respectively) were observed in each acid ester series. The antiallergic activity is modulated by hydrophobicity, and alkyl chain bulkiness.

Rosmarinic acid modulates the antioxidant status and protects pancreatic tissues from glucolipotoxicity mediated oxidative stress in high-fat diet: streptozotocin-induced diabetic rats.[Pubmed:25735949]

Mol Cell Biochem. 2015 Jun;404(1-2):143-59.

Persistent hyperglycemia and elevated levels of free fatty acids (FFA) contribute to oxidative stress, a proximate cause for the onset and progression of diabetes and its complications. The present study was hypothesized to evaluate the anti-diabetic potential of Rosmarinic acid (RA) during high-fat diet (HFD)-streptozotocin (STZ)-induced type 2 Diabetes (T2D) in wistar albino rats. Oral administration of RA (100 mg/kg b.w) significantly (p < 0.05) increased the insulin sensitivity index (ISI0,120), while the levels of blood glucose, HbA1c, advanced glycation end products (AGE), TNF-alpha, IL-1beta, IL 6, NO, p-JNK, P38 MAPK and NF-kappaB were significantly reduced, with a concomitant elevation in the plasma insulin levels in diabetic rats. Furthermore, RA treatment significantly (p < 0.05) reduced the levels of triglycerides, FFA and cholesterol in serum, and reduced the levels of lipid peroxides, AOPP's and protein carbonyls in the plasma and pancreas of diabetic rats. The diminished activities of pancreatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) and the decreased levels of plasma ceruloplasmin, vitamin C, vitamin E and reduced glutathione (GSH) in diabetic rats were also significantly (p < 0.05) recovered upon RA treatment denoting its antioxidant potential which was confirmed by Nrf-2, hemeoxyenase (HO-1) levels. Histological, ultrastructural and immunohistochemical data demonstrate that oral administration of RA protects pancreatic beta-cells from oxidative niche in HFD-STZ-induced experimental diabetes. Our findings suggest that the oral treatment with RA alleviates pancreatic beta-cell dysfunction and glucolipotoxicity-mediated oxidative stress during HFD-STZ-induced T2DM, perhaps through its antioxidant potential.

Antiepileptogenic, antioxidant and genotoxic evaluation of rosmarinic acid and its metabolite caffeic acid in mice.[Pubmed:25498895]

Life Sci. 2015 Feb 1;122:65-71.

AIMS: Antioxidant compounds have been extensively investigated as a pharmacological alternatives to prevent epileptogenesis. Rosmarinic acid (RA) and caffeic acid (CA) are compounds with antioxidant properties, and RA has been shown to inhibit GABA transaminase activity (in vitro). Our aim was to evaluate the effect of RA and CA on seizures induced by pentylenotetrazole (PTZ) using the kindling model in mice. MAIN METHODS: Male CF-1 mice were treated once every three days during 16days with RA (1, 2 or 4mg/kg; i.p.), or CA (1, 4 or 8mg/kg; i.p.), or positive controls diazepam (1mg/kg; i.p.) or vigabatrin (600mg/kg; p.o.), 30min before PTZ administration (50mg/kg; s.c.). After the last treatment, animals were sacrificed and the cortex was collected to evaluate free radicals (determined by 2',7'-dichlorofluorescein diacetate probe), superoxide dismutase (SOD) and genotoxic activity (Alkaline Comet Assay). KEY FINDINGS: Rosmarinic acid 2mg/kg increased latency and decreased percentage of seizures, only on the 4th day of observation. The other tested doses of RA and CA did not show any effect. Rosmarinic acid 1mg/kg, CA 4mg/kg and CA 8mg/kg decreased free radicals, but no dose altered the levels of enzyme SOD. In the comet assay, RA 4mg/kg and CA 4mg/kg reduced the DNA damage index. SIGNIFICANCE: Some doses of Rosmarinic acid and CA tested showed neuroprotective action against oxidative and DNA damage produced in the kindling epilepsy model, although they did not produce antiepileptogenic effect in vivo.

Multiple tyrosine metabolites are GPR35 agonists.[Pubmed:22523636]

Sci Rep. 2012;2:373.

Both kynurenic acid and 2-acyl lysophosphatidic acid have been postulated to be the endogenous agonists of GPR35. However, controversy remains whether alternative endogenous agonists exist. The molecular targets accounted for many nongenomic actions of thyroid hormones are mostly unknown. Here we report the agonist activity of multiple tyrosine metabolites at the GPR35. Tyrosine metabolism intermediates that contain carboxylic acid and/or catechol functional groups were first selected. Whole cell dynamic mass redistribution (DMR) assays enabled by label-free optical biosensor were then used to characterize their agonist activity in native HT-29. Molecular assays including beta-arrestin translocation, ERK phosphorylation and receptor internalization confirmed that GPR35 functions as a receptor for 5,6-dihydroxyindole-2-carboxylic acid, 3,3',5'-triiodothyronine, 3,3',5-triiodothyronine, gentisate, rosmarinate, and 3-nitrotyrosine. These results suggest that multiple tyrosine metabolites are alternative endogenous ligands of GPR35, and GPR35 may represent a druggable target for treating certain diseases associated with abnormality of tyrosine metabolism.

Inhibition of complement by covalent attachment of rosmarinic acid to activated C3b.[Pubmed:10353266]

Biochem Pharmacol. 1999 Jun 15;57(12):1439-46.

Rosmarinic acid has been reported to inhibit complement activation in vivo as well as in vitro. Previous studies suggested that the inhibitory effect was due to inhibition of C3/C5 convertases, but inhibition of C3b attachment would yield the same results. Recent work in our laboratory demonstrated that compounds with polyhydroxylated phenyl rings are highly reactive with the thioester bond in nascent C3b. These compounds block complement activation by preventing attachment of C3b to the activating surface. Because Rosmarinic acid contains two 3,4-dihydroxyphenyl groups, the current study was undertaken to re-examine the mechanism of inhibition by analyzing the effect of Rosmarinic acid on C3b attachment. In assays using purified complement proteins, Rosmarinic acid inhibited covalent attachment of C3b to cells with an 1C50 = 34 microM. Inhibition of C5 convertase activity required 1500 microM Rosmarinic acid, and no significant inhibition of the C3 convertase enzyme, which produces C3b from C3, was observed at 10,000 microM. In hemolytic assays using human serum, Rosmarinic acid was shown to inhibit activation of both the classical (IC50 = 180 microM) and the alternative (IC50 = 160 microM) pathways of complement. Rosmarinic acid concentrations up to 10,000 microM did not cause direct inactivation of C3. Radioiodination of Rosmarinic acid was used to demonstrate covalent activation-dependent incorporation of Rosmarinic acid specifically into the thioester-containing alpha'-chain of nascent C3b. These findings indicate that inhibition of complement activation by Rosmarinic acid is due to the reaction of Rosmarinic acid with the activated thioester of metastable C3b, resulting in covalent attachment of the inhibitor to the protein.

Modification of endotoxin-induced haemodynamic and haematological changes in the rabbit by methylprednisolone, F(ab')2 fragments and rosmarinic acid.[Pubmed:3838489]

Br J Pharmacol. 1985 Feb;84(2):317-27.

The effects of methylprednisolone, F(ab')2 fragments of human gamma globulins and Rosmarinic acid, an inhibitor of complement activation, were tested on endotoxin-induced haemodynamic and haematological changes in the rabbit. Their effects were compared with complement depletion by cobra venom factor (CVF) pretreatment. The results provide further evidence for the role of complement activation and the concomitant triggering of the arachidonic acid cascade in the early phase of shock. The formation of vasoactive prostanoids (prostacyclin and thromboxane A2), the arterial hypotension and the thrombocytopenia were largely dependent on the presence of the intact complement system. F(ab')2 fragments (150 mg kg-1, i.v.) diminished the second fall in blood pressure to some extent but failed to alter any of the other endotoxin-induced changes. Methylprednisolone (40 mg kg-1, i.v.) given 10 min before endotoxin significantly reduced the activation of complement, the second rise of prostacyclin and the secondary hypotension, but was without effect on the early thromboxane peak of the haematological features of endotoxin shock. Rosmarinic acid (20 mg kg-1, i.v.) may be of potential interest for treatment of septic shock, since the drug suppressed the endotoxin-induced activation of complement, the formation of prostacyclin, both hypotensive phases, the thrombocytopenia and the concomitant release of thromboxane A2. The role of leukocytes and their arachidonic acid metabolites in plasma exudation deserves further investigation, because leukopenia and pulmonary oedema were not complement-dependent and were not affected by any of the treatments. Our results indicate that drugs, interfering with complement activation and/or prostaglandin biosynthesis, may be beneficial in endotoxin shock, provided that they are administered at an early stage.

Description

Rosmarinic acid is a widespread phenolic ester compound in the plants. Rosmarinic acid inhibits MAO-A, MAO-B and COMT enzymes with IC50s of 50.1, 184.6 and 26.7 μM, respectively.

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