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    L-carnosine
    L-carnosine
    Information
    CAS No. 305-84-0 Price $40 / 20mg
    Catalog No.CFN93091Purity>=98%
    Molecular Weight226.23Type of CompoundAlkaloids
    FormulaC9H14N4O3Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: L-carnosine is an antioxidant naturally found in skeletal muscle, brain tissue, and the heart that protects cells against oxidative stress.L-carnosine plays an important role in inhibiting neuronal cell apoptosis through STAT3 signaling pathway after acute cerebral ischemia. L-carnosine may accelerate pressure ulcer healing during 4 weeks.
    Targets: NO | STAT | Pim | Bcl-2/Bax | Caspase
    In vivo:
    Med Sci Monit. 2014 Mar 11;20:399-405.
    L-carnosine alters some hemorheologic and lipid peroxidation parameters in nephrectomized rats.[Pubmed: 24614724]
    Chronic kidney disease (CKD) is a major health problem worldwide. Oxidative stress is one of the mediators of this disease. Systemic complications of oxidative stress are involved in the pathogenesis of hypertension, endothelial dysfunction, shortened erythrocyte lifespan, deformability, and nitric oxide (NO) dysfunction. L-carnosine is known as an antioxidant. In this study, our aim was to investigate the effect of carnosine on hemorheologic and cardiovascular parameters in CKD-induced rats.
    METHODS AND RESULTS:
    We used 4-month-old male Sprague-Dawley rats divided into 4 groups of 6 rats each. Three days after subtotal nephrectomy and sham operations, the surviving rats were divided into the 4 groups; 1) Sham (S), 2) Sham+Carnosine (S-C), 3) Subtotal nephrectomy (Nx), and 4) Subtotal nephrectomy + Carnosine (N-C). Carnosine was injected intraperitoneally (i.p.) (50 mg/kg) for 15 days. The control group received the same volume of physiological saline. In CKD rats, malondialdehyde (MDA) levels were increased, and NO and RBC deformability were decreased compared to Sham. Carnosine treatment decreased MDA levels, improved RBC (red blood cell) ability to deform, and increased NO levels. However, carnosine did not affect blood pressure levels in these rats.
    CONCLUSIONS:
    We found that carnosine has beneficial effects on CKD in terms of lipid peroxidation and RBC deformability. Carnosine may have a healing effect in microcirculation level, but may not have any effect on systemic blood pressure in CKD-induced rats.
    Exp Eye Res. 2013 Aug;113:135-42.
    Β-alanine and l-histidine transport across the inner blood-retinal barrier: potential involvement in L-carnosine supply.[Pubmed: 23773890]
    The supply of L-carnosine, a bioactive dipeptide of β-alanine and l-histidine, to the retina across the blood-retinal barrier (BRB) was studied.
    METHODS AND RESULTS:
    The in vivo and in vitro studies revealed low uptake activities for [(3)H]Gly-Sar, a representative dipeptide, suggesting that L-carnosine transport plays only a minor role at the BRB. The in vivo study using rats showed approximately 18- and 23-fold greater retinal uptake indexes (RUI) for [(3)H]β-alanine and [(3)H]l-histidine compared with that of a paracellular marker, respectively. The RUI of [(3)H]β-alanine was taurine- and γ-aminobutyric acid-sensitive, and the in vitro uptake by TR-iBRB2 cells showed time- concentration- and temperature-dependent [(3)H]β-alanine uptake, suggesting that a carrier-mediated process was involved in β-alanine transport across the inner BRB. [(3)H]β-Alanine uptake was inhibited by taurine and β-guanidinopropionic acid, suggesting that taurine transporter (TAUT/SLC6A6) is responsible for the influx transport of β-alanine across the inner BRB. Regarding l-histidine, the l-leucine-sensitive RUI of [(3)H]l-histidine was identified, and the in vitro [(3)H]l-histidine uptake by TR-iBRB2 cells suggested that a carrier-mediated process was involved in l-histidine transport across the inner BRB. The inhibition profile suggested that L-type amino acid transporter (LAT1/SLC7A5) is responsible for the influx transport of l-histidine across the inner BRB.
    CONCLUSIONS:
    These results show that the influx transports of β-alanine and l-histidine across the inner BRB is carried out by TAUT and LAT1, respectively, suggesting that the retinal L-carnosine is supplied by enzymatic synthesis from two kinds of amino acids transported across the inner BRB.
    Nutr Clin Pract. 2013 Oct;28(5):609-16.
    Effects of L-carnosine and its zinc complex (Polaprezinc) on pressure ulcer healing.[Pubmed: 23835365]
    L-carnosine (CAR) is an endogenous dipeptide. We aimed to determine the effects of CAR and its zinc complex polaprezinc (PLZ) on pressure ulcer healing in institutionalized long-term care patients.
    METHODS AND RESULTS:
    This study was a nonrandomized controlled trial with a maximum 4-week follow-up. Forty-two patients with stage II-IV pressure ulcers for 4 or more weeks were allocated to 1 of 3 groups in order of recruitment: the control group (n = 14) was untreated, the PLZ group (n = 10) orally received 150 mg/d PLZ (containing 116 mg CAR and 34 mg zinc), and the CAR group (n = 18) orally received 116 mg/d CAR. Pressure ulcer severity was measured weekly using the Pressure Ulcer Scale for Healing (PUSH) score. At baseline, no significant differences were found among groups in demographic and nutrition parameters and pressure ulcer characteristics (severity, size, and staging). After 4 weeks, the rate of pressure ulcer healing, assessed by the mean weekly improvement in PUSH score, was significantly greater in the CAR (1.6 ± 0.2, P = .02) and PLZ groups (1.8 ± 0.2, P = .009) than in the control group (0.8 ± 0.2). The difference between the CAR and PLZ groups was not significant (P = .73). Actual dietary intakes over this period did not differ significantly among groups.
    CONCLUSIONS:
    Our results suggest that CAR and PLZ may almost equally accelerate pressure ulcer healing during 4 weeks. The results need confirmation by randomized controlled trials with larger sample sizes.
    L-carnosine Description
    Source: The herbs of Geranium wilfordii Maxim.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.4203 mL 22.1014 mL 44.2028 mL 88.4056 mL 110.507 mL
    5 mM 0.8841 mL 4.4203 mL 8.8406 mL 17.6811 mL 22.1014 mL
    10 mM 0.442 mL 2.2101 mL 4.4203 mL 8.8406 mL 11.0507 mL
    50 mM 0.0884 mL 0.442 mL 0.8841 mL 1.7681 mL 2.2101 mL
    100 mM 0.0442 mL 0.221 mL 0.442 mL 0.8841 mL 1.1051 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Animal Research:
    Brain Res. 2013 Apr 24;1507:125-33.
    L-carnosine inhibits neuronal cell apoptosis through signal transducer and activator of transcription 3 signaling pathway after acute focal cerebral ischemia.[Pubmed: 23454231]
    Considerable studies have showed that L-carnosine provides anti-oxidative and anti-apoptotic roles in the animal models of global or focal cerebral ischemia. However, the anti-apoptotic mechanisms of L-carnosine in the focal cerebral ischemia model have yet to be elucidated.
    METHODS AND RESULTS:
    To investigate the molecular mechanisms, rat models of permanent middle cerebral artery occlusion (pMCAO) and sham operation were first established and then pMCAO and sham-operated rats were treated with L-carnosine or vehicle alone. After this treatment, neurological deficits were evaluated at 12, 24 and 72 h after operation and the infarct volume was measured at 72 h after treatment. In addition, we also detected the mRNA expression of signal transducer and activator of transcription 3 (STAT3) and Pim-1 and the protein expression of phosphorylated STAT3, Pim-1, bcl-2 and cleaved caspase-3 at 12, 24 and 72 h post-pMCAO. Our results showed that the L-carnosine-treated rats had milder neurological deficits and smaller infarct volume and showed up-regulated expression in mRNA levels of STAT3 and Pim-1 than vehicle-treated rats at 72 h after treatment. Meanwhile, compared with vehicle-treated rats, the L-carnosine-treated rats exhibited higher protein expressions of pSTAT3, Pim-1 and bcl-2 but lower expression of cleaved caspase-3 protein at 72 h following operation.
    CONCLUSIONS:
    These results indicate that L-carnosine plays an important role in inhibiting neuronal cell apoptosis through STAT3 signaling pathway after acute cerebral ischemia.
    Acta Medica (Hradec Kralove). 2013;56(1):23-8.
    The effect of L-carnosine on erythrocyte deformability and aggregation according to the cell age in young and aged rats.[Pubmed: 23909051]
    This study aimed to investigate alterations in hemorheology induced by L-carnosine, an anti- oxidant dipeptide, and to determine their relationship to oxidative stress in density-separated erythrocytes of aged and young rats.
    METHODS AND RESULTS:
    28 male Sprague Dawley rats were divided into 4 groups as aged (Aca), young (Yca) L-carnosine groups (250 mg/kg L-carnosine, i.p.) and aged (As), young (Ys) control groups (saline, i.p.). Density separation was further performed to these groups in order to separate erythrocytes according to their age. Blood samples were used for the determination of erythrocyte deformability, aggregation; and oxidative stress parameters. Erythrocyte deformability of Yca group measured at 0.53 Pa was lower than Aca group. Similarly, deformability of least-dense (young) erythrocytes of Yca group was decreased compared to least-dense erythrocytes of Aca groups. Total antioxidant capacity (TAC) of Aca group was higher and oxidative stress index (OSI) lower than As group.
    CONCLUSIONS:
    Although L-carnosine resulted in an enhancement in TAC of aged rats, this favorable effect was not observed in erythrocyte deformability and aggregation in the dose applied in this study.