Carnosic acid

CAS# 3650-09-7

Carnosic acid

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Quality Control of Carnosic acid

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Chemical structure

Carnosic acid

3D structure

Chemical Properties of Carnosic acid

Cas No. 3650-09-7 SDF Download SDF
PubChem ID 65126 Appearance White-yellowish powder
Formula C20H28O4 M.Wt 332.43
Type of Compound Diterpenoids Storage Desiccate at -20°C
Solubility DMSO : 130 mg/mL (391.06 mM; Need ultrasonic)
Chemical Name (4aR,10aS)-5,6-dihydroxy-1,1-dimethyl-7-propan-2-yl-2,3,4,9,10,10a-hexahydrophenanthrene-4a-carboxylic acid
SMILES CC(C)C1=C(C(=C2C(=C1)CCC3C2(CCCC3(C)C)C(=O)O)O)O
Standard InChIKey QRYRORQUOLYVBU-VBKZILBWSA-N
Standard InChI InChI=1S/C20H28O4/c1-11(2)13-10-12-6-7-14-19(3,4)8-5-9-20(14,18(23)24)15(12)17(22)16(13)21/h10-11,14,21-22H,5-9H2,1-4H3,(H,23,24)/t14-,20+/m0/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 Carnosic acid

1 Salvia sp.

Biological Activity of Carnosic acid

DescriptionCarnosic acid is a lipid absorption inhibitor, endowed with antioxidative, antimicrobial, photoprotective potential, and antiproliferative properties. It can protect neurons both in vitro and in vivo through activation of the Keap1/Nrf2 pathway via S-alkylation of targeted cysteines on Keap1. It is increasingly used within food, nutritional health and cosmetics industries.
TargetsNrf2 | LTR | Caspase | ROS | Antifection
In vitro

Carnosic acid inhibits TLR4-MyD88 signaling pathway in LPS-stimulated 3T3-L1 adipocytes.[Pubmed: 25324930]

Nutr Res Pract. 2014 Oct;8(5):516-20.

Carnosic acid (CA), found in rosemary (Rosemarinus officinalis) leaves, is known to exhibit anti-obesity and anti-inflammatory activities. However, whether its anti-inflammatory potency can contribute to the amelioration of obesity has not been elucidated. The aim of the current study was to investigate the effect of CA on Toll-like receptor 4 (TLR4) pathways in the presence of lipopolysaccharide (LPS) in 3T3-L1 adipocytes.
METHODS AND RESULTS:
3T3-L1 adipocytes were treated with CA (0-20 μM) for 1 h, followed by treatment with LPS for 30 min; mRNA expression of adipokines and protein expression of TLR4-related molecules were then measured. LPS-stimulated 3T3-L1 adipocytes showed elevated mRNA expression of tumor necrosis factor (TNF)-α, interleukin-6, and monocyte chemoattractant protein-1, and CA significantly inhibited the expression of these adipokine genes. LPS-induced up regulation of TLR4, myeloid differentiation factor 88, TNF receptor-associated factor 6, and nuclear factor-κB, as well as phosphorylated extracellular receptor-activated kinase were also suppressed by pre-treatment of 3T3-L1 adipocytes with CA.
CONCLUSIONS:
Results of this study suggest that CA directly inhibits TLR4-MyD88-dependent signaling pathways and decreases the inflammatory response in adipocytes.

Antimicrobial activity of Rosmarinus officinalis against oral pathogens: relevance of carnosic acid and carnosol.[Pubmed: 20658673 ]

Chem Biodivers. 2010 Jul;7(7):1835-40.

The in vitro inhibitory activity of crude EtOH/H2O extracts from the leaves and stems of Rosmarinus officinalis L. was evaluated against the following microorganisms responsible for initiating dental caries: Streptococcus mutans, S. salivarius, S. sobrinus, S. mitis, S. sanguinis, and Enterococcus faecalis.
METHODS AND RESULTS:
Minimum inhibitory concentrations (MIC) were determined with the broth microdilution method. The bioassay-guided fractionation of the leaf extract, which displayed the higher antibacterial activity than the stem extract, led to the identification of Carnosic acid (2) and carnosol (3) as the major compounds in the fraction displaying the highest activity, as identified by HPLC analysis. Rosmarinic acid (1), detected in another fraction, did not display any activity against the selected microorganisms. HPLC Analysis revealed the presence of low amounts of ursolic acid (4) and oleanolic acid (5) in the obtained fractions.
CONCLUSIONS:
The results suggest that the antimicrobial activity of the extract from the leaves of R. officinalis may be ascribed mainly to the action of 2 and 3.

In vivo

Protection from cyanide-induced brain injury by the Nrf2 transcriptional activator carnosic acid.[Pubmed: 25692407]

J Neurochem. 2015 Feb 18.

Cyanide is a life-threatening, bioterrorist agent, preventing cellular respiration by inhibiting cytochrome c oxidase, resulting in cardiopulmonary failure, hypoxic brain injury, and death within minutes. However, even after treatment with various antidotes to protect cytochrome oxidase, cyanide intoxication in humans can induce a delayed-onset neurological syndrome that includes symptoms of Parkinsonism. Additional mechanisms are thought to underlie cyanide-induced neuronal damage, including generation of reactive oxygen species. This may account for the fact that antioxidants prevent some aspects of cyanide-induced neuronal damage.
METHODS AND RESULTS:
Here, as a potential preemptive countermeasure against a bioterrorist attack with cyanide, we tested the CNS protective effect of Carnosic acid (CA), a pro-electrophilic compound found in the herb rosemary. CA crosses the blood-brain barrier to up-regulate endogenous antioxidant enzymes via activation of the Nrf2 transcriptional pathway. We demonstrate that CA exerts neuroprotective effects on cyanide-induced brain damage in cultured rodent and human-induced pluripotent stem cell-derived neurons in vitro, and in vivo in various brain areas of a non-Swiss albino mouse model of cyanide poisoning that simulates damage observed in the human brain. Cyanide, a potential bioterrorist agent, can produce a chronic delayed-onset neurological syndrome that includes symptoms of Parkinsonism. Here, cyanide poisoning treated with the proelectrophillic compound Carnosic acid, results in reduced neuronal cell death in both in vitro and in vivo models through activation of the Nrf2/ARE transcriptional pathway.
CONCLUSIONS:
Carnosic acid is therefore a potential treatment for the toxic central nervous system (CNS) effects of cyanide poisoning.

Carnosic acid, a catechol-type electrophilic compound, protects neurons both in vitro and in vivo through activation of the Keap1/Nrf2 pathway via S-alkylation of targeted cysteines on Keap1.[Pubmed: 17995931 ]

J Neurochem. 2008 Feb;104(4):1116-31.

Electrophilic compounds are a newly recognized class of redox-active neuroprotective compounds with electron deficient, electrophilic carbon centers that react with specific cysteine residues on targeted proteins via thiol (S-)alkylation. Although plants produce a variety of physiologically active electrophilic compounds, the detailed mechanism of action of these compounds remains unknown. Catechol ring-containing compounds have attracted attention because they become electrophilic quinones upon oxidation, although they are not themselves electrophilic.
METHODS AND RESULTS:
In this study, we focused on the neuroprotective effects of one such compound, Carnosic acid (CA), found in the herb rosemary obtained from Rosmarinus officinalis. We found that CA activates the Keap1/Nrf2 transcriptional pathway by binding to specific Keap1 cysteine residues, thus protecting neurons from oxidative stress and excitotoxicity. In cerebrocortical cultures, CA-biotin accumulates in non-neuronal cells at low concentrations and in neurons at higher concentrations.
CONCLUSIONS:
We present evidence that both the neuronal and non-neuronal distribution of CA may contribute to its neuroprotective effect. Furthermore, CA translocates into the brain, increases the level of reduced glutathione in vivo, and protects the brain against middle cerebral artery ischemia/reperfusion, suggesting that CA may represent a new type of neuroprotective electrophilic compound.

Carnosic acid attenuates renal injury in an experimental model of rat cisplatin-induced nephrotoxicity.[Pubmed: 21930180 ]

Food Chem Toxicol. 2011 Dec;49(12):3090-7.

Nephrotoxicity is one of the serious dose limiting side effects of cisplatin when used in the treatment of various malignant conditions. Accumulating evidence suggests that oxidative stress caused by free radicals and apoptosis of renal cells contributes to the pathogenesis of cisplatin-induced nephrotoxicity. Present study was aimed to explore the effect of Carnosic acid, a potent antioxidant, against cisplatin induced oxidative stress and nephrotoxicity in rats.
METHODS AND RESULTS:
A single dose of cisplatin (7.5mg/kg) caused marked renal damage, characterized by a significant (P<0.05) increase in serum creatinine, blood urea nitrogen (BUN) and relative weight of kidney with higher kidney MDA (malondialdehyde), tROS (total reactive oxygen species), caspase 3, GSH (reduced glutathione) levels and lowered tissue nitrite, SOD (superoxide dismutase), CAT (catalase), GSH-Px (glutathione peroxidase), GR (glutathione reductase) and GST (glutathione S-transferase) levels compared to normal control. Carnosic acid treatment significantly (P<0.05) attenuated the increase in lipid peroxidation, caspase-3 and ROS generation and enhanced the levels of reduced glutathione, tissue nitrite level and activities of SOD, CAT, GSH-Px, GR and GST compared to cisplatin control.
CONCLUSIONS:
The present study demonstrates that Carnosic acid has a protective effect on cisplatin induced experimental nephrotoxicity and is attributed to its potent antioxidant and antiapoptotic properties.

Protocol of Carnosic acid

Cell Research

Carnosic acid inhibits the proliferation and migration capacity of human colorectal cancer cells.[Pubmed: 22246562 ]

Oncol Rep. 2012 Apr;27(4):1041-8.

Cell lines:Human colon carcinoma cell lines, Caco-2, HT29 and LoVo
Concentrations: 0 to 388 μM
Incubation Time: 24 h
Method:
Cells (1×104) are seeded in 96-well microplates in complete medium. After 48 h, cells are washed twice with PBS and treated with RE, RA and CA (concentration range from 0 to 388 μM) in complete medium for 24 h. Cell viability is assessed.

Animal Research

Carnosic acid (CA) attenuates collagen-induced arthritis in db/db mice via inflammation suppression by regulating ROS-dependent p38 pathway.[Pubmed: 28343998]

Free Radic Biol Med. 2017 Jul;108:418-432.

Animal Models: Male C57BL/KsJ-db/db (db/db) mice
Formulation: DMSO
Dosages:30 mg/kg and 60 mg/kg
Administration: i.p.

Carnosic acid Dilution Calculator

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Preparing Stock Solutions of Carnosic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.0082 mL 15.0408 mL 30.0815 mL 60.163 mL 75.2038 mL
5 mM 0.6016 mL 3.0082 mL 6.0163 mL 12.0326 mL 15.0408 mL
10 mM 0.3008 mL 1.5041 mL 3.0082 mL 6.0163 mL 7.5204 mL
50 mM 0.0602 mL 0.3008 mL 0.6016 mL 1.2033 mL 1.5041 mL
100 mM 0.0301 mL 0.1504 mL 0.3008 mL 0.6016 mL 0.752 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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References on Carnosic acid

Protection from cyanide-induced brain injury by the Nrf2 transcriptional activator carnosic acid.[Pubmed:25692407]

J Neurochem. 2015 Jun;133(6):898-908.

Cyanide is a life-threatening, bioterrorist agent, preventing cellular respiration by inhibiting cytochrome c oxidase, resulting in cardiopulmonary failure, hypoxic brain injury, and death within minutes. However, even after treatment with various antidotes to protect cytochrome oxidase, cyanide intoxication in humans can induce a delayed-onset neurological syndrome that includes symptoms of Parkinsonism. Additional mechanisms are thought to underlie cyanide-induced neuronal damage, including generation of reactive oxygen species. This may account for the fact that antioxidants prevent some aspects of cyanide-induced neuronal damage. Here, as a potential preemptive countermeasure against a bioterrorist attack with cyanide, we tested the CNS protective effect of Carnosic acid (CA), a pro-electrophilic compound found in the herb rosemary. CA crosses the blood-brain barrier to up-regulate endogenous antioxidant enzymes via activation of the Nrf2 transcriptional pathway. We demonstrate that CA exerts neuroprotective effects on cyanide-induced brain damage in cultured rodent and human-induced pluripotent stem cell-derived neurons in vitro, and in vivo in various brain areas of a non-Swiss albino mouse model of cyanide poisoning that simulates damage observed in the human brain. Cyanide, a potential bioterrorist agent, can produce a chronic delayed-onset neurological syndrome that includes symptoms of Parkinsonism. Here, cyanide poisoning treated with the proelectrophillic compound Carnosic acid, results in reduced neuronal cell death in both in vitro and in vivo models through activation of the Nrf2/ARE transcriptional pathway. Carnosic acid is therefore a potential treatment for the toxic central nervous system (CNS) effects of cyanide poisoning. ARE, antioxidant responsive element; Nrf2 (NFE2L2, Nuclear factor (erythroid-derived 2)-like 2).

Carnosic acid inhibits TLR4-MyD88 signaling pathway in LPS-stimulated 3T3-L1 adipocytes.[Pubmed:25324930]

Nutr Res Pract. 2014 Oct;8(5):516-20.

BACKGROUND/OBJECTIVES: Carnosic acid (CA), found in rosemary (Rosemarinus officinalis) leaves, is known to exhibit anti-obesity and anti-inflammatory activities. However, whether its anti-inflammatory potency can contribute to the amelioration of obesity has not been elucidated. The aim of the current study was to investigate the effect of CA on Toll-like receptor 4 (TLR4) pathways in the presence of lipopolysaccharide (LPS) in 3T3-L1 adipocytes. MATERIALS/METHODS: 3T3-L1 adipocytes were treated with CA (0-20 microM) for 1 h, followed by treatment with LPS for 30 min; mRNA expression of adipokines and protein expression of TLR4-related molecules were then measured. RESULTS: LPS-stimulated 3T3-L1 adipocytes showed elevated mRNA expression of tumor necrosis factor (TNF)-alpha, interleukin-6, and monocyte chemoattractant protein-1, and CA significantly inhibited the expression of these adipokine genes. LPS-induced up regulation of TLR4, myeloid differentiation factor 88, TNF receptor-associated factor 6, and nuclear factor-kappaB, as well as phosphorylated extracellular receptor-activated kinase were also suppressed by pre-treatment of 3T3-L1 adipocytes with CA. CONCLUSIONS: Results of this study suggest that CA directly inhibits TLR4-MyD88-dependent signaling pathways and decreases the inflammatory response in adipocytes.

Antioxidant activity and mechanism of the abietane-type diterpene ferruginol.[Pubmed:25588148]

Nat Prod Res. 2015;29(18):1739-43.

The antioxidant activity of the abietane-type diterpene ferruginol was evaluated by comparison with that of Carnosic acid, ( +/- )-alpha-tocopherol and dibutylhydroxytoluene using 2,2-diphenyl-1-picrylhydrazyl, beta-carotene bleaching and linoleic acid assays. Ferruginol had the lowest antioxidant activity of this group using the 2,2-diphenyl-1-picrylhydrazyl and beta-carotene methods in polar solvent buffer. However, ferruginol exhibited stronger activity than Carnosic acid and alpha-tocopherol for linoleic acid oxidation under non-solvent conditions. Five peaks corresponding to ferruginol derivatives were detected through GC-MS analysis of the reaction between ferruginol and methyl linoleate. The three reaction products were identified as dehydroferruginol, 7beta-hydroxyferruginol and sugiol, and the other two peaks were assumed to be 7alpha-hydroxyferruginol and the quinone methide derivative of ferruginol. The time course of the reaction suggests that the quinone methide was produced early in the reaction and reacted further to produce dehydroferruginol, 7-hydroxyferruginol and sugiol. Thus, we inferred that quinone methide formation was a key step in the antioxidant reaction of ferruginol.

Carnosic acid.[Pubmed:25639596]

Phytochemistry. 2015 Jul;115:9-19.

Carnosic acid (salvin), which possesses antioxidative and antimicrobial properties, is increasingly exploited within the food, nutritional health and cosmetics industries. Since its first extraction from a Salvia species ( approximately 70 years ago) and its identification ( approximately 50 years ago), numerous articles and patents ( approximately 400) have been published on specific food and medicinal applications of Rosmarinus and Salvia plant extracts abundant in Carnosic acid. In contrast, relevant biochemical, physiological or molecular studies in planta have remained rare. In this overview, recent advances in understanding of Carnosic acid distribution, biosynthesis, accumulation and role in planta, and its applications are summarised. We also discuss the deficiencies in our understanding of the relevant biochemical processes, and suggest the molecular targets of Carnosic acid. Finally, future perspectives and studies related to its potential roles are highlighted.

Description

Carnosic acid has demonstrated inhibition of oxidative stress and inflammation, suppression of cell proliferation, and antibacterial activity.

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