Browsing by Author "Cicek, Haci Ahmet"

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The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the Trpm2 Channel
(Mdpi, 2025) Keles, Omer Faruk; Bayir, Mehmet Hafit; Cicek, Haci Ahmet; Ahlatci, Adem; Yildizhan, Kenan
This study investigated the protective effect of selenium (Se) in a cadmium (Cd)-induced nephrotoxicity model in rats and the role of the TRPM2 channel in this mechanism. For this purpose, Cd (25 mg/kg orally), Se (0.5 mg/kg i.p.), and 2-aminoethoxydiphenyl borate (2-APB), a TRPM2 channel antagonist, (3 mg/kg i.p.) were administered to rats every day for 5 days. At the end of the study, kidney tissues were analysed using histological and biochemical methods. A histopathological examination revealed congestion, tubular degeneration, necrosis, and glomerular adhesion in the Cd group. However, these lesions were significantly reduced in the Cd + Se and Cd + 2-APB groups, while the Cd + Se + 2-APB group showed a histological appearance similar to the control group. Immunohistochemical analysis revealed that Caspase-3, Bax, and TRPM2 expression was higher in the Cd group, while these levels were lower in the Se and 2-APB treatment groups (p < 0.05). Among the groups that received Cd, urea, creatinine, TOS, TNF-alpha, and IL-1 beta levels were at the highest level in the Cd group, while TAS level was at the lowest level (p < 0.05). The Se and 2-APB treatment modulated these parameters; however, Se + 2-APB treatment reduced urea, creatinine, TOS, TNF-alpha, and IL-1 beta levels to the lowest level compared to the Cd groups and brought the TAS level closer to the control group (p < 0.05). These findings indicated that targeting TRPM2 channel inactivation together with the selenium treatment could alleviate Cd-induced nephrotoxicity.
The Effects of Dexmedetomidine on Liver Injury in Rats With Experimental Sepsis: a Histopathological and Immunohistochemical Study
(Turkish Assoc Trauma Emergency Surgery, 2025) Keles, Omer Faruk; Kaplan, Havva Sayhan; Cicek, Haci Ahmet; Palabiyik, Onur; Yener, Zabit
BACKGROUND: In the rat sepsis model, the protective effect of dexmedetomidine (Dex) in sepsis-induced tissue injuries by reducing inflammation is still unclear. Research is ongoing to determine whether Dex modulates sepsis-induced tissue injury. The aim of this experimental study was to investigate the effect of Dex on liver injury in sepsis rats histopathologically and immunohistochemically. METHODS: In this study, sepsis was induced in rats by a 10 ml/kg E. coli injection, and the protective efficacy of Dex against liver damage was investigated through histopathological and immunohistochemical findings by the intraperitoneal administration of 100 mu g/ kg Dex. RESULTS: In our results, the most striking and basic morphological changes in the liver tissues of sepsis group rats were neutrophil leukocyte infiltrations in and around the vessels. In Dex-treated groups, neutrophil leukocyte infiltrations were more prominent, and marked dilatations were observed in the vessels. The fact that inflammatory reactions were more prominent in the Dex-treated groups was thought to be related to the increase in vascular permeability due to Dex's vasodilation effect. CONCLUSION: According to the histopathological and immunohistochemical findings obtained in the present study, we conclude that Dex did not alleviate sepsis-induced liver inflammation in a rat sepsis model.