. . .
Probably with some vasodilators to get it thoroughly dispersed and as close to the skin's surface as possible.
I was hoping that the endothelial cells lining the cardiovascular system would also be rejuvenated.
Yep; As Niner said above.
I was just thinking out load there:
If the Quercetin is killing of the endothelial cells lining the cardiovascular system; a vasodilator may be a good idea to get Quercetin into the microvasculature where circulation is at its lowest.
That would include all organs, but I was wondering if it would improve skin as that would be a good, easily examined, sign that it worked..
Quercetin which kills off senescent endothelial etc? cells is proven to be synergistic with Resveratrol which activates telomerase in endothelial progenitor cells.
I would have no problem taking another telomerase activator and vasodilator like Gingko Biloba at the same time as Quercetin and Resveratrol.
The dark horse is Dasatinib.
Is it synergistic with Quercetin, or do they just have an additive effect by killing of different senescent cell types?
Who knows how it will interact with Resveratrol and Gingko Biloba.
This Patent may sched some light and Dasatinib's MOA:
...Cells with inactive BRAF undergo senescence in the presence of dasatinib....
...In the present study, dasatinib induced senescence in HI 666 and Call2T cells but induced apoptosis in H661 cells into which were transfected kinase impaired BRAF mutations. Possible reasons for this discrepancy are that the absolute level of endogenous w BRAF, the level of mutant BRAF, or the w mutant BRAF ratio may influence the outcome of dasatinib- based treatment...
...The mechanism by which dasatinib induces senescence in NSCLC cells with kinase-deficient BRAF is unknown. It was hypothesized that dasatinib induces senescence by affecting CRAF function (8). Although it was found that dasatinib did not directly affect CRAF or BRAF kinase activity at relevant concentrations...
...Oncogene-induced senescence occurs after activation of oncogenes such as RAS and RAF. Classically, it is mediated by activation of the p^^/Rb and/or pi 4ARF/p53 tumor suppressor pathway. Senescence also can be induced and mediated by other pathways, such as those involving c-Src, STAT3, c-Myc, FOX04, Chk2, and c-Jun-N-terminal-kinase. In the present study, dasatinib induced senescence in HI 666 and Call2T cells but induced apoptosis in H661 cells into which were transfected kinase impaired BRAF mutations. Possible reasons for this discrepancy are that the absolute level of endogenous wtBRAF, the level of mutant BRAF, or the w mutant BRAF ratio may influence the outcome of dasatinib- based treatment. The level of mutant BRAF expression was higher in the transfected cells, which also harbored a full complement of endogenous "'BRAF, than in non-trans fected cells. [0081] Occasionally, spontaneous tumor regression occurs in melanoma and renal cell carcinoma cases and is thought to be immune mediated. Also, the activating V600EBRAF mutation in melanoma may induce an immune response. Although such a possibility cannot be excluded in the case of PX, spontaneous tumor regression is very rare in NSCLC cases. Instead, the dasatinib sensitivity of NSCLC cell lines with kinase impaired BRAF mutations is consistent with the patient having experienced a direct antitumor effect of dasatinib rather than an immune-mediated mechanism....
http://www.google.co...3155077A1?cl=en
...Dasatinib inhibited cell viability with an IC(50) in the submicromolar range in 7 of 10 tested cell lines. In sensitive cells, Dasatinib reduced anchorage-independent growth and, in some instances, induced senescence and apoptosis. In HTLA-230 cells, Dasatinib treatment caused down-regulation of c-Kit and c-Src phosphorylation in conjunction with strong inhibition of Erk1/2 and Akt activity...
http://www.pubfacts....n-orthotopic-mo