I really didn't want to get into a citations war where the results of one paper are immediately challenged by someone posting the results of a different or even contradictory study. I guess we all must make decisions as to which information we want to believe. Yes, cherry-picking, if you will. That said, I will cite below why I have decided to include Ursolic Acid in my daily regimen. If someone disagrees, fine, but as I have stated above, I won't participate in a “citation war.” You guys make your own decisions, but please remember that I am the messenger, not the message. Any disagreements, please direct them to the authors of the paper to let them respond.This disease has taken its toll, unfortunately, in defining who I am and I don't like it, but with many of us it is a matter of life and death, so in addition to the drugs we take courtesy of Big Pharma, most of us try, no matter how feeble (and laughable to some of our more learned members), with the goal of modestly affecting our conditioon in a positive way.
Inhibition of estrogen signaling through depletion of estrogen receptor alpha by ursolic acid and betulinic acid from Prunella vulgaris var. lilacina.
ABSTRACT
Extracts of Prunella vulgaris have been shown to exert antiestrogenic effects. To identify the compounds responsible for these actions, we isolated the constituents of P. vulgaris and tested their individual antiestrogenic effects. Rosmarinic acid, caffeic acid, ursolic acid (UA), oleanolic acid, hyperoside, rutin and betulinic acid (BA) were isolated from the flower stalks of P. vulgaris var. lilacina Nakai (Labiatae). Among these constituents, UA and BA showed significant antiestrogenic effects, measured as a decrease in the mRNA level of GREB1, an estrogen-responsive protein; the effects of BA were stronger than those of UA. UA and BA were capable of suppressing estrogen response element (ERE)-dependent luciferase activity and expression of estrogen-responsive genes in response to exposure to estradiol, further supporting the suppressive role of these compounds in estrogen-induced signaling. However, neither UA nor BA was capable of suppressing estrogen signaling in cells ectopically overexpressing estrogen receptor α (ERα). Furthermore, both mRNA and protein levels of ERα were reduced by treatment with UA or BA, suggesting that UA and BA inhibit estrogen signaling by suppressing the expression of ERα. Interestingly, both compounds enhanced prostate-specific antigen promoter activity. Collectively, these findings demonstrate that UA and BA are responsible for the antiestrogenic effects of P. vulgaris and suggest their potential use as therapeutic agents against estrogen-dependent tumors. Kim HI1, Quan FS2, Kim JE1, Lee NR1, Kim HJ1, Jo SJ1, Lee CM1, Jang DS3, Inn KS4.
mRNA which can be fragmented and faces the problem of being cleaved at weak spots [Reactive Sites]. Single Strand RNA is very much weaker in its molecular structure, than than the double helix[Double Strand] DNA.and has been implicated in regulating androgen receptors
Also when looking at estrogen receptors, ER-Alphas are in the intercellular structure of the PCa cell while the ER-Betas are on the membrane of the PCa Cell. There would be more concern as to actions allowing more androgens, specifically E2, access to the ER-Alphas, than the membrane ER-Betas.
If if you can prevent protein encoding for the growth of PCa cells, and keep Estradiol from the ER-Alphas, and some of the ER-Betas---the RNA will not have which to carry to the PCa cell Receptors---since Estradiol is the androgen most likely to do the most harm.
“The estrogen receptor beta (ERβ) is the most prevalent ER in the human prostate, while the estrogen receptor alpha (ERα) is restricted to basal cells of the prostatic epithelium and stromal cells. In high grade prostatic intraepithelial neoplasia (HGPIN), the ERα is up-regulated and most likely mediates carcinogenic effects of estradiol as demonstrated in animal models. The partial loss of the ERβ in HGPIN indicates that the ERβ acts as a tumor suppressor. The tumor promoting function of the TMPRSS2-ERG fusion, a major driver of prostate carcinogenesis, is triggered by the ERα and repressed by the ERβ. The ERβ is generally retained in hormone naïve and metastatic prostate cancer, but is partially lost in castration resistant disease. Prostate. 2018 Jan;78(1):2-10. doi: 10.1002/pros.23446. Epub 2017 Nov 2. Estrogen receptor signaling in prostate cancer: Implications for carcinogenesis and tumor progression.”
