1 ‫السورتوين‬ ‫تعبير‬ ‫على‬ ‫واالستروجني‬ ‫األندروجينات‬ ‫تأثير‬ ‫دراسة‬ ‫األهداف:‬ .)HAECs(‫البشرية‬ ‫األبهرية‬ ‫البطانية‬ ‫اخلاليا‬ ‫في‬)SIRT1(‫مدار‬ ‫على‬ SIRT-1 ‫لتعبير‬ ‫البلمرة‬ ‫سلسلة‬ ‫تفاعل‬ ‫حتليل‬ ‫أجري‬ ‫املنهجية:‬ ،)DHEA(‫من‬ ‫مختلفة‬ ‫بتركيزات‬ ‫املعاجلة‬ HAECs ‫في‬)h(‫ساعة‬ 48 ‫االستروجني)‬ ‫(هرمون‬)E3(‫و‬)E2(،)E1(‫واالستروجني‬ ‫واألندروجني‬ ‫املرتفع‬ ‫اجللوكوز‬ ‫تأثير‬ ‫كذلك‬ ‫فحصنا‬ ‫الزمنية.‬ ‫الدورات‬ ‫اجلرعة-تبعية‬ ‫لدراسة‬ ‫واإلستروجني.‬ ‫األندروجينات‬ ‫عن‬ ‫الناجم‬ SIRT1 ‫تعبير‬ ‫على‬ ‫وهرمون‬ ‫واالستروجني،‬ ‫واألندروجني‬ ،)DHEA(‫أنتجت‬ ‫النتائج:‬ SIRT1 ‫تعبير‬ ‫في‬ ‫اجلرعة‬ ‫على‬ ‫تعتمد‬ ‫وبزيادة‬ ‫ملحوظ‬ ‫بشكل‬ ‫التستوستيرون‬ ‫ملم)‬ 40(‫املرتفع‬ ‫للجلوكوز‬ ‫كان‬ ‫02ميكروغرام/مل.‬ ‫إلى‬ 10 ‫نطاق‬ ‫في‬ ‫01ميكروغرام/‬ ‫عن‬ ‫الناجت‬ SIRT1 ‫تعبير‬ ‫على‬ ‫ملحوظ‬ ‫بشكل‬ ‫مثبطة‬ ‫تأثيرات‬ ‫زيادة‬ ‫في‬ ،E3 ‫ليس‬ ‫ولكن‬ ، E2 ‫و‬ ‫االستروجني‬ ‫تسبب‬ .)p=0.024(‫مل‬ ‫ميكروغرام/‬ 20 ‫إلى‬ 10 ‫من‬ SIRT1 ‫تعبير‬ ‫في‬ ‫اجلرعة‬ ‫على‬ ‫تعتمد‬ ‫ملحوظة‬ ‫تعبير‬ ‫كبير‬ ‫بشكل‬ ‫مينع‬ ‫لم‬ ‫اجللوكوز‬ ‫من‬ ‫ملم‬ 40 ‫أو‬ ‫ملم‬ 20 ‫مع‬ ‫العالج‬ ‫مل.‬ ‫كال‬ ‫أكد‬ ‫ذلك،‬ ‫ومع‬ ‫التحكم؛‬ ‫وسيط‬ ‫في‬ E3 ‫و‬ E1 ‫عن‬ ‫الناجم‬ SIRT1 E2 ‫عن‬ ‫الناجم‬ SIRT1 ‫تعبير‬ ‫على‬ ‫كبير‬ ‫بشكل‬ ‫للجلوكوز‬ ‫املرتفعني‬ ‫الوسطني‬ ‫التوالي.‬ ‫على‬ ،)p=0.007، p=0.005(‫التحكم‬ ‫وسط‬ ‫في‬ E1 ‫و‬ ‫واالستروجني‬ ‫األندروجني‬ ‫و‬ DHEA ‫أن‬ ‫إلى‬ ‫النتائج‬ ‫هذه‬ ‫تشير‬ ‫اخلالصة:‬ ‫اجللوكوز‬ ‫متوسط‬ ‫إن‬ .HAECs ‫في‬ SIRT1 ‫تعبير‬ ‫بالتأكيد‬ ‫ينشطون‬ E2 ‫و‬ ‫احلد‬ ‫ميكن‬ ‫ال‬ ‫فإنه‬ ، ‫ذلك‬ ‫ومع‬ ‫؛‬ ‫األساسي‬ ‫اجليني‬ ‫التعبير‬ ‫لتثبيط‬ ‫فعال‬ ‫املرتفع‬ .HAECs ‫في‬ ‫قوية‬ ‫واالستروجني‬ ‫األندروجني‬ ‫عن‬ ‫الناجم‬ SIRT1 ‫التعبير‬ ‫من‬ Objectives: To investigate the effect of androgens and estrogens on surtuin 1 (SIRT1) expression in human aortic endothelial cells (HAECs). Methods: Real-time polymerase chain reaction analysis of SIRT-1 expression over 48 hours (h) was performed in HAECs treated with various concentrations of dehydroepiandrostendione (DHEA), androstenedione and testosterone (androgens), estrone (E1), estradiol (E2), and estriol (E3) (estrogens) to investigate the dose-dependency of time courses. The influence of high glucose on SIRT1 expression induced by the androgens and estrogens was also examined. Results: Dehydroepiandrostendione, androstenedione, and testosterone remarkably Original Article produced a dose-dependent increase in SIRT1 expression in the range of 10 to 20 µg/ml. High glucose (40mM) medium had significantly inhibitory effects on 10 µg/ml DHEA-induced SIRT1 expression (p=0.024). Estrone and E2, but not E3, caused a marked dose-dependent increase in SIRT1 expression from 10 to 20 µg/ml. Treatment with 20 mM or 40 mM glucose medium did not significantly inhibit E1and E3-induced SIRT1 expression in control medium; however, both high glucose mediums significantly emphasized E2-induced SIRT1 expression in control medium (p=0.007, p=0.005). Conclusion: These results suggest that DHEA, androstenedione, testosterone, E1, and E2 definitely activate SIRT1 expression in HAECs. A high glucose medium is potent to inhibit the basa...

Background/Aim: Curcumin is a natural compound of turmeric, which inhibits prostate cancer cell proliferation. This study examined whether treatment of LNCaP prostate cancer cells with the combination of curcumin and dutasteride, a 5-alpha reductase inhibitor, affect proliferation and the amount of testosterone and dihydrotestosterone. Materials and Methods: LNCaP Cells were incubated with curcumin or the combination of curcumin and dutasteride and cell proliferation was measured at 72 h. LC-MS/MS was used to determine testosterone and dihydrotestosterone concentrations in prostate cancer cells. Results: Curcumin combined with dutasteride suppressed proliferation and affected apoptosis of LNCaP cells. The combination of curcumin and dutasteride also reduced the amount of testosterone and dihydrotestosterone in LNCaP cells. The secretion of prostate-specific antigen was inhibited by the combination treatment in a dose-dependent manner. Conclusion: Treatment with the combination of curcumin and dutasteride may interfere with the intra-tumoral androgen activity.