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    Effects of Ozone Therapy on Cyclophosphamide-induced Urinary Bladder Toxicity in Rats
    (Canadian Soc Clinical Investigation, 2013) Tasdemir, Seda; Tasdemir, Cemal; Vardi, Nigar; Ates, Burhan; Taslidere, Elif; Karaaslan, Merve G.; Sapmaz, Hilal I.
    Purpose: This study investigated the efficacy of ozone therapy (OT) in a rat model of cyclophosphamide-induced hemorrhagic cystitis (HC). Methods: Forty Wistar Albino male rats were divided into five groups: sham, OT, cyclophosphamide (CP), OT+CP and CP+OT. Hemorrhagic cystitis (HC) was induced by intraperitoneal (i.p) administration a single dose of 100 mg/kg CP. OT was performed once daily for three days. the CP+OT group received OT (0.2 mg/kg) i.p 24 h after CP administration. CP was injected to the OT+CP group the day after the third course of OT. All animals were killed four days after CP administration. Bladder injury and oxidative stress parameters were determined from tissue samples. Results: We found small, but non-statistically significant biochemical and histological changes in the animals treated with OT alone. CP administration induced cystitis, as manifested by a marked loss of urothelial cells, as well as hemorrhaging and edema in the bladder as determined by histopathological examination. It also caused a significant decrease in the endogenous antioxidant compound glutathione (GSH) and elevation of lipid peroxidation, and nitric oxide (NO) and myeloperoxidase (MPO) levels in the rats' urinary bladder tissue. OT was able to ameliorate these changes; however these effects were prominent in the CP+OT group when compared with the OT+CP group.: For example, the NO level in the CP+OT group was 68% of the OT+CP group (p < 0.05). Conclusion: OT prevented CP-induced urothelial damage by diminishing bladder oxidative stress, inflammation and NO levels. OT may help to ameliorate bladder damage induced by CP in the clinical setting.
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    Investigating the possible protective effect of caffeic acid phenethyl ester on aquaporin-2 changes in renal ischemia-reperfusion injury in rats
    (Mexican Acad Surgery, 2025) Sapmaz, Hilal I.; Kose, Evren; Karaca, Zeynal M.; Akyurek, Sema; Parlakpinar, Hakan; Deresoy, Faik A.; Turkoz, Yusuf
    Objective: We aimed to investigate the changes in renal aquaporins (AQP) of rats in renal ischemia-reperfusion (I/R) injury and the protective effects of caffeic acid phenethyl ester (CAPE) against these changes. Methods: Forty-five adult rats were divided into six groups: control, sham (right nephrectomy), I/R (right nephrectomy + left kidney I/R), I/R+CAPE (I/R procedure after i.p. CAPE), sham + CAPE, and sham + dimethyl sulfoxide. Blood urea nitrogen, Cr, and K+ levels were measured in the sera. Tissues were stained with hematoxylin and eosin for histopathological examination. For immunohistochemical analysis, AQP2 was applied using the streptavidin/biotin/peroxidase system. AQP2 gene expression in kidney tissues was examined by polymerase chain reaction (PCR). Results: In the I/R, congestion, inflammation, and necrosis were found to increase compared to the control. In the I/R+CAPE, improvement was observed in necrosis compared to the I/R. There was a decrease in AQP2 expression in the I/R. In PCR, no significant difference was observed in AQP2 gene expression between the I/R and control and between the I/R+CAPE and I/R. Conclusion: Renal I/R inhibits the production of AQP2 in the kidney and causes histological and biochemical damage. CAPE administration before I/R has a protective effect on the kidney.