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EN
We compared the intensity of staining of interstitial cells (ICs) and neural tissue in the lower urinary tract of rabbits with diabetes with the intensity in normal subjects. Diabetes was induced by injecting alloxane (65mg/kg) in adult male rabbits. After 3 days, rabbits with a blood glucose level >300 mg/dL were considered to have diabetes. After 8 weeks, the rabbits were killed, and tissue specimens from the bladder, prostate and urethra were obtained. ICs were stained with anti-human CD117 (c-kit) rabbit polyclonal antibody, and neural tissue was stained with synaptophysin. The streptavidin-biotin method was used for immunohistochemical staining. The intensity of c-kit and synaptophysin staining were scored as negative (0), weak (+), moderate (++), and strong (+++). Staining intensity of ICs and neural tissue was assessed and compared in tissues obtained from rabbits with diabetes (n=8) and from control subjects (n=7). Although staining intensity of both ICs and neural tissue was found to be significantly decreased in the bladder tissue of rabbits with diabetes compared to that in the control group (p=0.0001 [ICs] and p=0.021 [neural tissue]), no significant differences in staining intensity of ICs and neural tissue in the urethra and in the prostate was found when rabbits with diabetes were compared to the control group. Diabetes may cause dysfunction of the lower urinary tract, particularly in the urinary bladder, as shown by the staining intensity of ICs and neural tissue.
EN
Results of in vivo and in vitro experiments have demonstrated the presence of a local renin-angiotensin system (RAS) in the prostate. However, the role of this system in the physiology and pathology of the prostate is still unclear. Recent reports have indicated that RAS is also involved in the regulation of cell proliferation, differentiation, migration as well as angiogenesis, inflammation and apoptosis, which suggests its important role in carcinogenesis. Reorganization of individual elements of the renin-angiotensin system has been reported in both benign prostatic hyperplasia and prostate cancer. These changes concerned the expression of AT1 receptor, angiotensin converting enzyme (ACE) and local concentration of angiotensin II or angiotensinogen. This review focuses on the role of RAS in the induction and progression of prostate cancer as well as on the analysis of potential benefits of RAS modulation in anticancer therapy.
PL
Wyniki badań in vivo oraz in vitro ujawniły obecność lokalnego układu renina-angiotensyna (RAS) w gruczole krokowym, niemniej jednak rola tego układu zarówno w fizjologii jak i patologii stercza nadal nie jest dobrze znana. Najnowsze doniesienia wskazują, że RAS obok swojej klasycznej roli jest zaangażowany w proliferację, różnicowanie i migrację komórek, angiogenezę, procesy zapalne oraz apoptozę, co sugeruje jego istotny udział w procesie kancerogenezy. Reorganizacja poszczególnych elementów RAS została odnotowana zarówno w łagodnym rozroście jak i nowotworach złośliwych gruczołu krokowego. Powyższe zmiany dotyczyły między innymi, poziomu receptora AT1, ekspresji enzymu konwertującego angiotensynę I jak również lokalnego stężenia angiotensyny II i angiotensynogenu. Niniejsza praca ma na celu podsumowanie dotychczasowej wiedzy odnośnie udziału RAS w zapoczątkowaniu i późniejszym rozwoju raka stercza, jak również przeanalizowanie potencjalnych korzyści wynikających z modulacji RAS w kontekście terapii antynowotworowej.
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