|Description:||1. Simvastatin possesses potent anti-inflammatory property. |
2. Simvastatin reduces burn-induced splenic apoptosis via downregulation of the TNF-α/NF-κB pathway.
3. Simvastatin rescues Aβ-mediated cerebrovascular and cognitive deficits in a transgenic mouse model of AD.
4. Simvastatin induces p65 instability leads to MMP-9 down-regulation in leukemia cells, while Simvastatin induces JNK1/c-Jun/ATF-2 activation maintains the MMP-2 expression underlying p65 down-regulation.
5. Simvastatin has potent benefits on endothelial and smooth muscle cell-mediated vasomotor responses, endothelial NO synthesis and in preserving capillary integrity; is an FDA-approved cholesterol-lowering medication and can inhibit STAT1 activation in vitro.
|Targets:||TNF-α | NF-kB | MMP(e.g.TIMP) | p65 | JNK | Beta Amyloid | TGF-β/Smad | NO | NOS | STAT | IFN-γ|
|Source:||From Penicillium Citrinum|
|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.
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|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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.3891 mL||11.9457 mL||23.8914 mL||47.7829 mL||59.7286 mL|
|5 mM||0.4778 mL||2.3891 mL||4.7783 mL||9.5566 mL||11.9457 mL|
|10 mM||0.2389 mL||1.1946 mL||2.3891 mL||4.7783 mL||5.9729 mL|
|50 mM||0.0478 mL||0.2389 mL||0.4778 mL||0.9557 mL||1.1946 mL|
|100 mM||0.0239 mL||0.1195 mL||0.2389 mL||0.4778 mL||0.5973 mL|
Ann Surg. 2015 May;261(5):1006-12.
|Simvastatin reduces burn injury-induced splenic apoptosis via downregulation of the TNF-α/NF-κB pathway.[Pubmed: 24950285 ]|
|OBJECTIVE: Recent studies have suggested that epidermal burn injuries are associated with inflammation and immune dysfunction. Simvastatin has been shown to possess potent anti-inflammatory properties. Thus, we hypothesized that Simvastatin protects against burn-induced apoptosis in the spleen via its anti-inflammatory activity. METHODS: Wild-type, tumor necrosis factor alpha knockout (TNF-α KO) and NF-κB KO mice were subjected to full-thickness burn injury or sham treatment. The mice then were treated with or without Simvastatin, and the spleen was harvested to measure the extent of apoptosis. Expression levels of TNF-α and NF-κB were also determined in spleen tissue and serum. RESULTS: Burn injury induced significant splenic apoptosis and systemic cytokine production. Simvastatin protected the spleen from apoptosis, reduced cytokine production in the serum, and increased the survival rate. Simvastatin decreased burn-induced TNF-α and NF-κB expression in the spleen and serum. TNF-α and NF-κB KO mice demonstrated lower levels of apoptosis in spleen in response to burn injury. Simvastatin did not further decrease burn-caused apoptosis and mortality in either strain of KO mice. CONCLUSIONS: Simvastatin reduces burn-induced splenic apoptosis via downregulation of the TNF-α/NF-κB pathway.|
Biochem Pharmacol. 2014 Dec 15;92(4):530-43.
|Simvastatin induces NFκB/p65 down-regulation and JNK1/c-Jun/ATF-2 activation, leading to matrix metalloproteinase-9 (MMP-9) but not MMP-2 down-regulation in human leukemia cells.[Pubmed: 25316568]|
|The aim of the present study was to explore the signaling pathways associated with the effect of Simvastatin on matrix metalloproteinase-2 (MMP-2)/MMP-9 expression in human leukemia K562 cells. In sharp contrast to its insignificant effect on MMP-2, Simvastatin down-regulated MMP-9 protein expression and mRNA levels in K562 cells. Simvastatin-induced Pin1 down-regulation evoked NFκB/p65 degradation. Meanwhile, Simvastatin induced JNK-mediated c-Jun and ATF-2 activation. Over-expression of Pin1 suppressed Simvastatin-induced MMP-9 down-regulation. Treatment with SP600125 (a JNK inhibitor) or knock-down of JNK1 reduced MMP-2 expression in Simvastatin-treated cells. Simvastatin enhanced the binding of c-Jun/ATF-2 with the MMP-2 promoter. Down-regulation of c-Jun or ATF-2 by siRNA revealed that c-Jun/ATF-2 activation was crucial for MMP-2 expression. Suppression of p65 activation or knock-down of Pin1 by shRNA reduced MMP-2 and MMP-9 expression in K562 cells. Over-expression of constitutively active JNK1 rescued MMP-2 expression in Pin1 shRNA-transfected cells. Simvastatin treatment also suppressed MMP-9 but not MMP-2 expression in human leukemia U937 and KU812 cells. Taken together, our data indicate that Simvastatin-induced p65 instability leads to MMP-9 down-regulation in leukemia cells, while Simvastatin-induced JNK1/c-Jun/ATF-2 activation maintains the MMP-2 expression underlying p65 down-regulation.|
J Cereb Blood Flow Metab. 2015 Mar;35(3):512-20.
|Simvastatin restored vascular reactivity, endothelial function and reduced string vessel pathology in a mouse model of cerebrovascular disease.[Pubmed: 25564230]|
|We recently found that Simvastatin rescued Aβ-mediated cerebrovascular and cognitive deficits in a transgenic mouse model of AD. However, whether Simvastatin can counteract Aβ-independent deficits remains unknown. Here, we evaluated the effects of Simvastatin in aged TGF mice on cerebrovascular reactivity and structure, and on cognitive performance. Simvastatin restored baseline levels of nitric oxide (NO), NO-, and KATP channel-mediated dilations and endothelin-1-induced contractions. Simvastatin significantly reduced vasculopathy with arteriogenic remodeling and string vessel pathology in TGF mice. In contrast, Simvastatin did not lessen gliosis, and the cerebrovascular levels of pro-fibrotic proteins and calcification markers remained elevated after treatment. The TGF mice displayed subtle cognitive decline that was not affected by Simvastatin. Our results show potent benefits of Simvastatin on endothelial- and smooth muscle cell-mediated vasomotor responses, endothelial NO synthesis and in preserving capillary integrity. We conclude that Simvastatin could be indicated in the treatment of cerebrovascular dysfunction associated with VaD and AD|
J Invest Dermatol. 2015 Apr;135(4):1080-8.
|Simvastatin prevents and reverses depigmentation in a mouse model of vitiligo.[Pubmed: 25521459]|
|Simvastatin, an FDA-approved cholesterol-lowering medication, inhibited STAT1 activation in vitro. Therefore, we hypothesized that Simvastatin may be an effective treatment for vitiligo. We found that Simvastatin both prevented and reversed depigmentation in our mouse model of vitiligo, and reduced the number of infiltrating autoreactive CD8(+) T cells in the skin. Treatment of melanocyte-specific, CD8(+) T cells in vitro decreased proliferation and IFN-γ production, suggesting additional effects of Simvastatin directly on T cells. Based on these data, Simvastatin may be a safe, targeted treatment option for patients with vitiligo.|