Tanshinone IIA-sulfonic sodium

Tanshinone IIA-sulfonic sodium
Product Name Tanshinone IIA-sulfonic sodium
CAS No.: 69659-80-9
Catalog No.: CFN90399
Molecular Formula: C19H17O6S.Na
Molecular Weight: 396.39 g/mol
Purity: >=98%
Type of Compound: Diterpenoids
Physical Desc.: Red powder
Targets: Akt | FOXO3A | Bim | Calcium Channel
Source: The roots of Salvia miltiorrhiza
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $40/20mg
Tanshinone IIA sulfonate (sodium) is a water-soluble derivative of tanshinone IIA, which acts as an inhibitor of store-operated Ca2+ entry (SOCE), and is used to treat cardiovascular disorders.Sodium tanshinone IIA sulfonate pretreatment reduces infarct size and improves cardiac function in an ischemia-reperfusion-induced rat myocardial injury model via activation of Akt/FOXO3A/Bim-mediated signal pathway.
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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.

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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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    Tanshinone IIA sodium sulfonate protects against cardiotoxicity induced by doxorubicin in vitro and in vivo.[Pubmed: 19358873 ]
    Although doxorubicin (DXR) is an effective antineoplastic agent; the serious cardiotoxicity mediated by the production of reactive oxygen species has remained a considerable clinical problem. Our hypothesis is that Tanshinone IIA-sulfonic sodium (TSNIIA-SS), which holds significant affects on cardioprotection in clinic, protects against DXR-induced cardiotoxicity.
    METHODS AND RESULTS:
    In vitro investigation on H9c2 cell line, as well as in vivo study in animal model of DXR-induced chronic cardiomyopathy were performed. TSNIIA-SS significantly increased cell viability and ameliorated apoptosis of DXR-injured H9c2 cells using CCK-8 assay and Hoechst 33342 stain respectively. Furthermore, the cardio-protective effects of TSNIIA-SS were confirmed with decreasing ST-interval and QRS interval by electrocardiography (ECG); improving appearance of myocardium with haematoxylin and eosin (H&E) stain; increasing myocardial tensile strength using tension to rupture (TTR) assay and decreasing fibrosis through picric-sirius red staining comparing with those receiving DXR alone.
    CONCLUSIONS:
    These data have provided the considerable evidences that TSNIIA-SS is a protective agent against DXR-induced cardiac injury.
    《Strait Pharmaceutical Journal》 2010-05
    Influence of tanshinone on glutamic acid content in spinal cord and serum in a rat model of spinal cord ischemia/reperfusion injury[Reference: WebLink]
    To explore the interventional effect of tanshinone on glutamic acid content in spinal cord and in serum and neurological function in a rat model of spinal cord ischemia/reperfusion injury.
    METHODS AND RESULTS:
    A total of 88 Sprague Dawley rats were randomly divided into a sham operation(n=8),model(n=40),and tanshinone(n=40) groups.Abdominal aorta occlusion was performed along the right renal arterial root using a Scoville-Lewis clamp to induce spinal cord ischemia.Blood flow was recovered 30 minutes following occlusion to establish models of spinal cord ischemia/reperfusion injury.Abdominal aorta occlusion was not performed in the sham operation group.An intraperitoneal injection of Tanshinone IIA-sulfonic sodium solution was administered to rats in the tanshinone group,preoperatively.In addition,rats in the sham operation and model groups were treated with an intraperitoneal injection of the same concentration of saline,preoperatively.Tirty minutes after ischemia,rats in the model and tanshinone groups were observed at 30min,hour1,4,8,and 12 following perfusion,with eight rats for each time point.After cutting the spinal cord and drawing the blood from inferior vena cava at each time point we detected glutamic acid content in spinal cord and glutamic acid content in serum.At hour 4,8,and 12 following perfusion,evaluated neurological fuction using Tarlov method in model and tanshinone groups. All 88 rats were included in the final analysis.Glutamic acid content in spinal and serum of model and tanshinone groups rose ischemia/reperfusion injury 30min later,reached a peak 4 hours after reperfusion,fall-off thenceforth,and put back 12 hours after reperfusion.
    CONCLUSIONS:
    Tanshinone could reduce glutamic acid content in spinal cord and protected neurological function in a rat model of spinal cord ischemia/reperfusion injury.
    Zhong Yao Cai. 2007 Jul;30(7):811-5.
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    To study the preventive effect of Sodium Tanshinone II A sulfonic acid (Tanshinone IIA-sulfonic sodium)on intimal by perplasia in rabbit iliac artery balloon injury model and explore the possible mechanism.
    METHODS AND RESULTS:
    Thirty male pure breed Nexw Zealand white rabbits were un-dertaken experimental balloon injury in left iliac artery. Then the rabbits were assigned into treatment group (n=15) and control group (n=15), paired with weights. Sodium Tanshinone II A sulfonie acid had been injected intraxenously with 7.5 - 9 mg/day for 6 days in treatment group. Saline of equivalence was given in contol group. The balloon injured arteries were harvested in the 7th, 14th, and 28th days after balloon injury, and Paraffin sections were made. At last, HE staining, apoptosis TUNEL assay were undertaken. (1) HE staining analysis: Media and intimal areas in treatment group at 14th day post-operation were larger than that in the 7th day (P = 0.003 and < 0.001, respectively). Media and intimal areas in treatment group decreased at the 28th day post-operation, while increased in control. Both media and intimal areas were significantly different (P < 0.001 respectively. (2) Tunel analysis discovered that, apoptosis reached peak in both treatment and control groups at the 28th post-operation. Differences of apoptosis cells counts in media and intimal between treatment and control groups were non-significant at the 7th, and 28th days, while differences at the 14th day were significant (p = 0.031 and 0.029 respectively). Apoptosis cells counting in treatment group at the 14th day increased more dramatically than that in the control.
    CONCLUSIONS:
    Intravenous Sodium Tanshinone II A sulfonic acid inhibites intimal proliferation after arterial balloon injury in rabbits. The effect can he partially explained by the induction of apoptosis in injured artery. Clinical effect of tanshinone II A still needs further evaluation. Sodium TA-II A sulfonic acid may be of potential therapeutic value in the prevention of restenosis after angioplasty.
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