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    Salvianolic acid A
    Information
    CAS No. 96574-01-5 Price $128 / 20mg
    Catalog No.CFN99161Purity>=98%
    Molecular Weight494.45Type of CompoundPhenylpropanoids
    FormulaC26H22O10Physical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Salvianolic acid A Description
    Source: The root of Salvia miltiorrhiza Bge.
    Biological Activity or Inhibitors: 1. Salvianolic acid A has protection against cerebral lesion, defense from oxidative damage and improvement of remembrance; it also has antithrombotic effect, antiplatelet action and can modulate hemorheology without affecting coagulation system, the mechanisms underlying such activities may involve the induction of cAMP.
    2. Salvianolic acid A possesses antioxidant activity, also has a significant protective effect against isoproterenol-induced myocardial infarction; it activates the Nrf2/HO-1 axis in RPE cells and protects against oxidative stress via activation of Akt/mTORC1 signaling.
    3. Salvianolic acid A (oral) can significantly improve glucose metabolism and inhibit oxidative injury as well as protect against impaired vascular responsiveness in STZ-induced diabetic rats.
    4. Salvianolic acid A has protection on oxidative stress and liver injury induced by carbon tetrachloride in rats, which may mainly be related to its antioxidative effect.
    5. Salvianolic acid A inhibits platelet activation via the inhibition of PI3K, and attenuates arterial thrombus formation in vivo, suggests that it may be developed as a novel therapeutic agent for the prevention of thrombotic disorders.
    6. Salvianolic acid A is a novel matrix metalloproteinase-9 inhibitor, can prevents cardiac remodeling in spontaneously hypertensive rats.
    7. Salvianolic acid A inhibits PDGF-BB-activated HSC proliferation, partially through apoptosis induction, it exerts no direct cytotoxicity on primary hepatocytes and HSC-T6 cells under experimental concentrations.
    Solvent: Pyridine, Methanol, Ethanol, 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.
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.0224 mL 10.1122 mL 20.2245 mL 40.449 mL 50.5612 mL
    5 mM 0.4045 mL 2.0224 mL 4.0449 mL 8.0898 mL 10.1122 mL
    10 mM 0.2022 mL 1.0112 mL 2.0224 mL 4.0449 mL 5.0561 mL
    50 mM 0.0404 mL 0.2022 mL 0.4045 mL 0.809 mL 1.0112 mL
    100 mM 0.0202 mL 0.1011 mL 0.2022 mL 0.4045 mL 0.5056 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.
    Salvianolic acid A References Information
    Citation [1]

    Phytomedicine. 2014 Oct 15;21(12):1725-32.

    Salvianolic acid A reverses paclitaxel resistance in human breast cancer MCF-7 cells via targeting the expression of transgelin 2 and attenuating PI3 K/Akt pathway.[Pubmed: 25442283]
    In addition, Salvianolic acid A effectively prevented transgelin 2 and adenosine-triphosphate binding cassette transporter (ABC transporter) including P-glycoprotein (P-gp), multidrug resistance associated protein 1 (MRP1), and breast cancer resistance protein (BCRP) up-regulation and exhibited inhibitory effect on PI3 K/Akt signaling pathway in MCF-7/PTX cells. Taken together, Salvianolic acid A can reverse paclitaxel resistance through suppressing transgelin 2 expression by mechanisms involving attenuation of PI3 K/Akt pathway activation and ABC transporter up-regulation. These results not only provide insight into the potential application of Salvianolic acid A in reversing paclitaxel resistance, thus facilitating the sensitivity of breast cancer chemotherapy, but also highlight a potential role of transgelin 2 in the development of paclitaxel resistance in breast cancer.
    Citation [2]

    Anticancer Drugs. 2015 Feb;26(2):210-23.

    Salvianolic acid A shows selective cytotoxicity against multidrug-resistant MCF-7 breast cancer cells.[Pubmed: 25419632]
    We have shown that Salvianolic acid A inhibited proliferation, caused cell cycle arrest at the S phase, and induced apoptosis dose dependently to the two kinds of cancer cells. However, the resistant cells were significantly susceptible to the inhibition of Salvianolic acid A compared with the parental cells. Salvianolic acid A increased the level of reactive oxygen species (ROS) by 6.2-fold in the resistant cells, whereas the level of Salvianolic acid A-induced ROS changed only by 1.6-fold in their parental counterparts. Thus, the data showed that the selective cytotoxicity resulted from the hypersensitivity of the resistant cells to the strongly elevated ROS by Salvianolic acid A. In addition, Salvianolic acid A-triggered apoptosis was associated with increased caspase-3 activity, disrupted mitochondrial membrane potential, downregulated Bcl-2 expression, and upregulated Bax expression in the resistant cells. Moreover, Salvianolic acid A downregulated the level of P-glycoprotein, which was overexpressed in the resistant cells. This indicated that Salvianolic acid A modulated MDR. Furthermore, Salvianolic acid A showed higher antitumor activity than did doxorubicin in xenografts established from the resistant cells. The present work raised a possibility that Salvianolic acid A might be considered a potential choice to overcome MDR for the selective susceptibility of the resistant breast cancer cells to Salvianolic acid A treatment.
    Citation [3]

    J Ethnopharmacol. 2014 Sep 29;155(3):1589-96.

    Prevention of pulmonary fibrosis with salvianolic acid a by inducing fibroblast cell cycle arrest and promoting apoptosis.[Pubmed: 25102244]
    BLM-treated rats exhibited increased alveolar wall thickness and collagen deposition in lung tissues, but these pathologies were greatly attenuated by daily administration of Salvianolic acid A. We also found that Salvianolic acid A significantly inhibited the proliferation, adhesion and migration of fibroblasts in vitro. This was partly due to a strong induction of cell cycle arrest and apoptosis upon Salvianolic acid A treatment. Consistent with these phenotypes, we observed decreased expression of the cell cycle-related proteins cyclin D1, cyclin E1, and cyclin B1, and increased expression of p53 and p21 in Salvianolic acid A-treated cells. In addition, the anti-apoptotic Bcl-2 protein decreased in a dose-dependent manner, while cleaved caspase-3 protein increased upon Salvianolic acid A treatment.
    Citation [4]

    PLoS One. 2014 Jul 14;9(7):e102292.

    The anti-apoptotic and cardioprotective effects of salvianolic acid a on rat cardiomyocytes following ischemia/reperfusion by DUSP-mediated regulation of the ERK1/2/JNK pathway.[Pubmed: 25019380]
    Our results showed that LDH, MIA and cell apoptosis were decreased, and various parameters of heart function were improved by Salvianolic acid A pretreatment and SP application. In the I/R group, the expression levels of p-ERK1/2 and DUSP4/16 were not significantly different compared with the CON group, however, the protein expression levels of p-ERK1/2, Bcl-2 and DUSP4/16 were higher, while p-JNK, Bax, caspase 3 and DUSP2 levels were reduced among the Salvianolic acid A+I/R, PD+Salvianolic acid A+I/R and SP+I/R groups. The above indices were not significantly different between the Salvianolic acid A+I/R and SP+I/R groups. Compared with the Salvianolic acid A+I/R group, p-ERK1/2 was increased and p-JNK was decreased in the Salvianolic acid A+si-DUSP2+I/R, however, p-ERK was downregulated and p-JNK was upregulated in Salvianolic acid A+si-DUSP4+I/R group. Salvianolic acid A exerts an anti-apoptotic role against myocardial IRI by inhibiting DUSP2-mediated JNK dephosphorylation and activating DUSP4/16-mediated ERK1/2 phosphorylation.
    Citation [5]

    J Cardiovasc Pharmacol. 2014 Oct;64(4):318-25.

    Salvianolic acid A suppresses CCL-20 expression in TNF-α-treated macrophages and ApoE-deficient mice.[Pubmed: 24853487]
    Recombinant tumor necrosis factor-α (TNF-α) upregulated CCL-20 production in dose- and time-dependent manners in RAW264.7 cells. The activity of TNF-α-induced CCL-20 production seemed to be significantly suppressed by Salvianolic acid A. Using p38 mitogen-activated protein kinase inhibitor, we found that p38 mediated the effects of TNF-α- and Salvianolic acid A-induced CCL-20 expression changes. In addition, immunohistochemical analysis of aortic root of ApoE mice also demonstrated that the expressions of CCL-20 and CCR6 were both downregulated significantly with Salvianolic acid A treatment. Furthermore, treatment of Salvianolic acid A inhibited the progression of the atherosclerotic plaques and lipid accumulation.
    Citation [6]

    Biomed Rep. 2013 Mar;1(2):213-217.

    Salvianolic acid A positively regulates PTEN protein level and inhibits growth of A549 lung cancer cells.[Pubmed: 24648921]
    Salvianolic acid A (Sal A) is an effective compound extracted from Salvia miltiorrhiza which has been used in the treatment of various diseases. Preliminary data indicate that Sal A treatment has a specific anti-lung cancer effect. However, the manner in which Sal A regulates cancer growth remains unknown. In this study, the A549 lung cancer cell line and its response to Sal A treatment was examined. Results showed that Sal A treatment significantly decreased A549 cell growth, promoted partial apoptosis and increased mitochondrial membrane permeability. Western blot analysis showed that Sal A upregulated the phosphatase and tensin homolog (PTEN) protein level, while consistently downregulating Akt phosphorylation. These results indicate that Sal A negatively mediates A549 lung cancer cell line growth or apoptosis, most likely by positively regulating PTEN protein level.