Hallo zusammen,
ich habe hier eine spannende Fragestellung an euch, und zwar möchte ich einen nM Wert des Stoffes THC (tetrahydrocannabinol) in entsprechende Nanogramm THC pro Milliliter Blut umwandeln. Spannend ist die Frage vor allem aufgrund seriöser Studien, die starke Hinweise darauf geben, dass extrem geringe Mengen THC eine entscheidende Rolle bei der Forschung nach Medikamtenen gegen Morbus Alzheimer spielen könnten. Wer sich tiefer mit dem Thema befassen möchte, findet hier einen hochinteressanten Artikel: http://journal.frontiersin.org/artic...014.00037/full. Meine Frage bezieht sich auf eine Studie der University of South Florida, die im April 2014 im Journal of Alzheimers Disease veröffentlicht wurde.
Frage: Gibt es eine Möglichkeit herauszufinden, welche Menge (ng) THC im Blut einer Person equivalent ist zu einer Konzentration von 0.25 nM THC in folgender Lösung:
HFIP pretreated A1-40 peptide was obtained from Biomer Technology, California. In thioflavin T (ThT) solutions (1.6 µg/ml dissolved in 20mM Tris-HCL), THC solution was prepared at concentration of 250, 25, 2.5, and 0.25 nM.THCsolutionwas added containing ThT buffer into black 96 well plates. Unaggregated βA peptide solution was thawed, diluted, and immediately
added to wells, making the final concentration of A1-40 at 1µM.
Abstrakt:
The purpose of this study was to investigate the potential therapeutic qualities of Delta 9-tetrahydrocannabinol (THC) with respect to slowing or halting the hallmark characteristics of Alzheimer’s disease. N2a-variant amyloid-Beta - protein precursor (APP) cells were incubated with THC and assayed for amyloid-Beta (ABeta) levels at the 6-, 24-, and 48-hour time marks. THC was also tested for synergy with caffeine, in respect to the reduction of the A-Beta level in N2a/A-BetaPPswe cells. THC was also tested to determine if multiple treatments were beneficial. The MTT assay was performed to test the toxicity of THC. Thioflavin T assays and western blots were performed to test the direct anti-A-Beta aggregation significance of THC. Lastly, THC was tested to determine its effects on glycogen synthase kinase-3 (GSK-3) and related signaling pathways. From the results, we have discovered THC to be effective at lowering A-Beta levels in N2a/APPswe cells at extremely low concentrations in a dose-dependent manner. However, no additive effect was found by combining caffeine and THC together. We did discover that THC directly interacts with A-Beta peptide, thereby inhibiting aggregation. Furthermore, THC was effective at lowering both total GSK-3 levels and phosphorylated GSK-3 in a dose-dependent manner at low concentrations. At the treatment concentrations, no toxicity was observed and the CB1 receptor was not significantly upregulated. Additionally, low doses of THC can enhance mitochondria function and does not inhibit melatonin’s enhancement of mitochondria function. These sets of data strongly suggest that THC could be a potential therapeutic treatment option for Alzheimer’s disease through multiple functions and pathways.
Ich würde mich freuen, hier ein paar Ansätze zur Umrechnung zu finden. Vielen Dank im Voraus für eure Antworten.
Federik