Name : Rosemary Extract Carnosic acid
Source: Rosemary ?
Botanical Name : Rosmarinus officinalis
Extract part: Leaf?
Composition : Carnosic acid
Appearance: Fine Brownish Yellow powder
Country of origin:P.R. China
Rosmarinus officinalis L. from Lamiaceae family, is commonly known as rosemary.?Rosemary is a widely cultivated herbal plant that is originated in the Mediterranean area. Rosemary is an aromatic evergreen shrub with leaves similar to?hemlock?needles .The leaves are used as a flavoring in foods and a prescription for treating minor ailments including :gout, cough, headache, high blood pressure, and reducing age-related memory loss.
Rosemary is used topically for preventing and treating baldness by applying to the skin ; and treating circulation problems, toothache, a skin condition called eczema, and joint or muscle pain such as myalgia, sciatica, and intercostal neuralgia. It is also used for wound healing, in bath therapy (balneotherapy), and as an insect repellent.
Rosemary contains a number of phytochemicals, including rosmarinic acid, camphor, caffeic acid, ursolic acid, betulinic acid, rosmanol and the antioxidants carnosic acid and carnosol.
Rosmarinic acid is a chemical compound firstly found in Rosmarinus officinalis which has antioxidant properties.
Another main antioxidant in rosemary is the phenolic diterpene carnosic acid ,appears to be the main substance for general oxidation leading to artifacts withγ-or δ-lactone structure in extracts of Rosmarinus officinalis .
Rosmarinic acid is a caffeic acid ester of salvianic acid A that acts as a GABA transaminase inhibitor, more specifically on 4-aminobutyrate transaminase.Rosmarinic acid also inhibits the expression of indoleamine 2,3-dioxygenase via its cyclooxygenase-inhibiting properties.
Constituents in Rosemary extracts from Rosmarinus officinalis L contains several compounds proven to have antioxidative function.Early investigation proved that carnosol and carnosic acid have been suggested to account for over 90% of the antioxidant properties of rosemary extract.Purified carnosol and carnosic acid are powerful inhibitors of lipid peroxidation in microsomal and liposomal systems, more effective than propyl gallate.Carnosol and carnosic acid are good scavengers of peroxyl radicals (CCl3O2) generated by pulse radiolysis, with calculated rate constants of 1–3 × 106M-1?S-1?and 2.7 × 107M-1?S-1?respectively.Carnosic acid reacted with HOCl in such a way as to protect the protein α1-antiproteinase against inactivationand appears to scavenge H2O2, but it could also act as a substrate for the peroxidase system.Both carnosol and carnosic acid stimulated DNA damage in the bleomycin assay but they scavenged hydroxyl radicals in the deoxyribose assay. The calculated rate constants for reaction with ·OH in the deoxyribose system for carnosol and carnosic acid were 8.7 × 1010M-1?and 5.9 × 1010M-1?S-1respectively.Moreover they also reduce cytochrome c but with a rate constant significantly lower than that of O-.2.
Biosci Biotechnol Biochem.?reported in 2007 supercritical fluid SF-CO2 treatment of Rosemarinus officinalis L. fresh leaves under optimum conditions (80 degrees C at 5,000 psi) yielded 5.3% of extract supercritical fluid extraction (SFE)-80, in which five major active principles were identified by liquid chromatography/mass spectrometry (LC/MS), viz., rosmarinic acid, carnosol, 12-methoxycarnosic acid, carnosic acid, and methyl carnosate.
When treated in RAW 264.7, apparent dose-dependent NO inhibition. SFE-80 exhibited dose-dependent viability suppression and significant tumor necrosis factor alpha (TNF-alpha) production in Hep 3B, whereas no effect was found in Chang liver cells. Furthermore, no effect was observed in RAW 264.7 at dosages of 3.13 to 25 microg/ml, indicating that SFE-80 exhibited a noncytotoxic character. Conclusively, rosemary can be considered an herbal anti-inflammatory and anti-tumor agent.
Carnosic acid, a phenolic diterpene, exhibited potent antioxidant and anticancer properties in both in vivo and in vitro conditions?.Recent research examined whether carnosic acid could sensitize TRAIL-mediated apoptosis in human renal carcinoma Caki cells.Research found that carnosic acid markedly induced TRAIL-mediated apoptosis in human renal carcinoma (Caki, ACHN, and A498), and human hepatocellular carcinoma (SK-HEP-1), and human breast carcinoma (MDA-MB-231) cells, but not normal cells (TMCK-1 and HSF). Carnosic acid induced down-regulation of c-FLIP and Bcl-2 expression at the post-translational levels, and the over-expression of c-FLIP and Bcl-2 markedly blocked carnosic acid-induced TRAIL sensitization. Furthermore, carnosic acid induced death receptor (DR)5, Bcl-2 interacting mediator of cell death (Bim), and p53 up-regulated modulator of apoptosis (PUMA) expression at the transcriptional levels via CCAAT/enhancer-binding protein-homologous protein (CHOP). Down-regulation of CHOP expression by siRNA inhibited DR5, Bim, and PUMA expression, and attenuated carnosic acid plus TRAIL-induced apoptosis.In conclusion,study demonstrates that carnosic acid enhances sensitization against TRAIL-mediated apoptosis through the down-regulation of c-FLIP and Bcl-2 expression, and up-regulation of ER stress-mediated DR5, Bim, and PUMA expression at the transcriptional levels.
Study on Human respiratory syncytial virus (hRSV) revealed the bioactive ?constituent of an extract of?Rosmarinus officinalis,carnosic acid , exerted a strong inhibitory effect against hRSV infection.
Among the tested bioactive constituents of?R. officinalis, carnosic acid displayed the most potent anti-hRSV activity and was effective against both A- and B-type viruses. Carnosic acid efficiently suppressed the replication of hRSV in a concentration-dependent manner. Carnosic acid effectively suppressed viral gene expression without inducing type-I interferon production or affecting cell viability, suggesting that it may directly affect viral factors. A time course analysis showed that addition of carnosic acid 8 hours after infection still effectively blocked the expression of hRSV genes, further suggesting that carnosic acid directly inhibited the replication of hRSV.
The importance of free radical-induced oxidative damage after traumatic brain injury (TBI) has been well documented. Despite multiple clinical trials with radical-scavenging antioxidants that are neuroprotective in TBI models, none is approved for acute TBI patients. As an alternative antioxidant target, Nrf2 is a transcription factor that activates expression of antioxidant and cytoprotective genes by binding to antioxidant response elements (ARE) within DNA.Researchers hypothesized that administration of carnosic acid (CA) would reduce oxidative damage biomarkers in brain tissue and also preserve cortical mitochondrial respiratory function post-TBI. A mouse controlled cortical impact (CCI) model was employed with a 1.0mm cortical deformation injury. Administration of CA at 15 minutes post-TBI reduced cortical lipid peroxidation, protein nitration, and cytoskeletal breakdown markers in a dose-dependent manner at 48 hours post-injury. Moreover, CA preserved mitochondrial respiratory function compared to vehicle animals. This was accompanied by decreased oxidative damage to mitochondrial proteins, suggesting the mechanistic connection of the two effects. Lastly, delaying the initial administration of CA up to 8 hours post-TBI was still capable of reducing cytoskeletal breakdown, thereby demonstrating a clinically relevant therapeutic window for this approach. This study demonstrates that pharmacological Nrf2-ARE induction is capable of neuroprotective efficacy when administered after TBI.
Carnosic acid is known to has multiple potent biochemical activities including antioxidant,antiviral ,anticancer and anti-inflammatory.Researches suggested that Carnosic acid has potential application in medical treatment .