Tıp Fakültesi

Permanent URI for this communityhttps://hdl.handle.net/20.500.12514/3075

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Citation - WoS: 6
Citation - Scopus: 5
Effects of Acute Carbon Monoxide Poisoning on Liver Damage and Comparisons of Related Oxygen Therapies in a Rat Model
(Taylor & Francis Ltd, 2024) Demirtas, Berjan; Taskin, Seyhan; Gokdemir, Gul Sahika; Seker, Ugur
Acute carbon monoxide (CO) poisoning may cause liver damage and liver dysfunction. Therefore, in this study, we aimed to compare the efficiency of normobaric oxygen (NBO) and high-flow nasal cannula oxygen (HFNCO) treatments on liver injury. For that purpose, 28 male Wistar albino rats were divided into four groups (Control, CO, CO + NBO, and CO + HFNCO). The control group was allowed to breath room air for 30 min. Acute CO poisoning in CO, CO + NBO, CO + HFNCO was induced by CO exposure for 30 min. Thereafter, NBO group received 100% NBO with reservoir mask for 30 min. HFNCO group received high-flow oxygen through nasal cannula for 30 min. At the end of the experiment, all animals were sacrificed by cardiac puncture under anesthesia. Serum liver function tests were measured. Liver tissue total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) levels, tissue histomorphology and immunoexpression levels of Bax, Caspase 3, TNF-alpha, IL-1 beta, and NF-kappa B were also examined. Our observations indicated that acute CO poisoning caused significant increases in blood COHb, serum aminotransferase (AST), alanine aminotransferase (ALT0, alkaline phosphatase (ALP), total protein, albumin, and globulin levels but a decrease in albumin to globulin ratio (all, p < 0.05). Furthermore, acute CO poisoning significantly increased the OSI value, and the immunoexpresssion of Bax, Caspase 3, TNF-alpha, IL-1 beta, and NF-kappa B in liver tissue (all, p < 0.05). These pathological changes in serum and liver tissue were alleviated through both of the treatment methods. In conclusion, both the NBO and HFNCO treatments were beneficial to alleviate the acute CO poisoning associated with liver injury and dysfunction. [GRAPHICS] .
Citation - WoS: 12
Citation - Scopus: 10
The Nephroprotective Effect of Quercetin in Cyclophosphamide-Induced Renal Toxicity Might Be Associated With Mapk/Erk and Nf-Κb Signal Modulation Activity
(Taylor & Francis Ltd, 2024) Kavak, Deniz Evrim; Dokumaci, Fatma Zehra; Kizildag, Sefa; Irtegun-Kandemir, Sevgi; Seker, Ugur
The present study aimed to examine the protective effect of quercetin (QUE) on cyclophosphamide (CTX)-induced nephrotoxicity. For that purpose, 24 mice were divided into four groups (Control, QUE, CTX, and CTX + QUE). The CTX and CTX + QUE groups received 200 mg/kg of cyclophosphamide on the 1(st) and 7(th) days. The QUE and CTX + QUE groups were treated with 50 mg/kg of quercetin daily for 14 days. At the end of the experiment, the animals were sacrificed, and kidney samples were analyzed. The results indicated that CTX leads to severe morphological degenerations and disruption in renal function. Serum BUN, Creatinine, Uric acid, tissue Bax, Caspase 3, TNF-alpha and IL-1 beta expression levels were upregulated in the CTX group compared to Control and QUE groups (p < 0.05). Although MAPK/ERK phosphorylation level is not affected in CTX group, there was a significant increase in CTX + QUE group (p < 0.05), but the NF-kappa B was significantly suppressed in this group (p < 0.01). The RT-qPCR results showed that the cyt-c and the Bax/Bcl-2 ratio mRNA expression folds were upregulated in the CTX group (p < 0.01), which was downregulated in the CTX + QUE group. However, there was a significant difference in the CTX + QUE group compared to the Control and QUE groups (p < 0.01). The findings showed that administering quercetin along with cyclophosphamide alleviated renal injury by regulating apoptotic and inflammatory expression. Moreover, the administration of quercetin and cyclophosphamide could synergistically improve renal function test results, and activate cellular responses, which upmodulate MAPK/ERK phosphorylation and suppression of NF-kappa B.
Citation - WoS: 7
Citation - Scopus: 8
Oxidative stress, apoptosis, inflammation, and proliferation modulator function of visnagin provide gonadoprotective activity in testicular ischemia-reperfusion injury
(Verduci Editore srl, 2023) Sağır, Süleyman; Şeker, Uğur; Pekince Özener, Merve; Yüksel, Meral; Demir, Mehmet
OBJECTIVE: Visnagin (Vis) is a compound found in the flowers and seeds of the Ammi visnaga plant with promising antioxidant and anti-inflammatory properties. We aimed to investigate the dose-dependent gonadoprotective effects of visnagin in rats while considering oxidative stress, apoptosis, and inflammation-related protein expression levels. MATERIALS AND METHODS: Twenty-eight adult rats were divided into four groups of seven animals each; control, ischemia/reperfusion (I/R), I/R+30Vis, and I/R+60Vis. Animals in control received no surgical application and were sacrificed at the end of the experiment. The rats in I/R, I/R + Vis30, and I/R + Vis60 were exposed to testicular ischemia and the animals in I/R + Vis30, and I/R + Vis60 groups received either 30 or 60 mg/kg visnagin intraperitoneal. At the end of the experiment, testis tissues were used for the measurement of oxidative stress, apoptosis, and inflammation. RESULTS: Our microscopic examinations indicated that I/R resulted in testicular degenerations and morphological alterations, which were improved in visnagin-treated animals. The biochemical analyses demonstrated that oxidative stress in the I/R group increased significantly (p<0.05) compared to the control group. The immunohistochemical examinations showed that pro-apoptotic Bax and Caspase 3 expressions, and pro-inflammatory tumor necrosis factor-alpha (TNF-α) levels were significantly up-regulated (p<0.05) but proliferating nuclear antigen (PCNA) levels in I/R group was significantly (p<0.001) down-regulated compared to the control group. CONCLUSIONS: Ischemia leading to testicular torsion is a reproductive health-affecting problem, and current surgical treatment methods might be insufficient to recover the testis due to the accumulation of reactive oxygen species (ROS). Our observations indicate that visnagin is a potential co-modality along with the surgical interventions for the recovery of ischemia encountered testis, but we believe the requirement of more detailed studies to explore the underlying signaling pathways and the strength of visnagin against testicular ischemia-reperfusion injury.

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