Browsing by Author "Demir, Mehmet"

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Citation - WoS: 34
Citation - Scopus: 32
Investigation of oxidant/antioxidant and anti-inflammatory effects of apigenin on apoptosis in sepsis-induced rat lung
(Journal of Biochemical and Molecular Toxicology, 2021) Unsal, Velid; Çiçek, Mustafa; Doganer, Adem; Demir, Mehmet
We suppose that apigenin may inhibit the cellular process of sepsis-induced lung injury, which is considered to be a major cause of morbidity and mortality, and may improve inflammation and oxidative stress. The aim of this study was to investigate the potential protective effect of apigenin in a rat model of polymicrobial sepsis. Eight groups consisting of a total of 64 female Wistar albino rats were used for this study. Pro-inflammatory (TNF-α, IL-1-β, IL-6) and anti-inflammatory (TGF-β, IL-10) cytokine levels were measured with the enzyme-linked immunosorbent assay technique, oxidant/antioxidants parameters were measured using the spectrophotometric method and Bax and Caspase-3 immunohistochemical methods. TNF-α, TGF-β, IL-1β, and IL-6 levels significantly increased in the sepsis-induced group than in the control groups, while IL-10 levels decreased. Lipid peroxidase (LPO), an oxidative stress marker, increased, while the antioxidant defense parameters of superoxide dismutase (SOD), catalase (CAT) activities, glutathione (GSH) levels decreased. Although Bax and Caspase-3 immunoreactivity and H score levels significantly increased in the sepsis group, significant decreases were found in the groups treated with apigenin. In conclusion, we are of the opinion that apigenin treatment improves lung injury by inhibiting oxidative stress and inflammatory cell damage.
Nephroprotective Effects of Visnagin through Modulation of Macrophage Polarization, Oxidative Stress, Inflammation and Apoptosis in Renal I/R Injury
(de Gruyter Poland SP z o o, 2026) Pekince-Ozoner, Merve; Seker, Ugur; Kaya, Seval; Yuksel, Meral; Demir, Mehmet; Sagir, Suleyman; Gokdemir, Gul Sahika
Objectives: The study aimed to investigate the nephroprotective effects of visnagin on renal ischemia-reperfusion (I/R) injury and the role of M1/M2 macrophage polarization in this process. Methods: Forty-two adult rats were divided into six groups: Control, Visnagin30 mg/kg, Visnagin60 mg/kg, I/R, I/R + Visnagin30 mg/kg, I/R + Visnagin60 mg/kg (n=7). Bilateral renal ischemia was induced by clamping for 25 min, followed by 2 h of reperfusion. Visnagin or vehicle was administered to the animals intraperitoneally 2 h before reperfusion. At the end of the study, kidney samples were collected for analysis of oxidative stress, inflammatory cytokines, apoptotic protein expression, and M1/M2 macrophage polarization. Results: I/R injury increased malondialdehyde (MDA), chemiluminescence (CL), IL-1 beta, and IL-6 levels while decreasing glutathione (GSH) in renal tissue, indicating enhanced oxidative stress (p<0.001) and inflammation (p<0.05). Histopathological examination showed glomerular atrophy, tubular degeneration, and intertubular hemorrhage. Visnagin treatment at 60 mg/kg significantly reduced MDA, CL, and IL-1 beta levels, and increased GSH (p<0.05). Immunohistochemically, visnagin decreased Bax (p<0.001), caspase-3 (p<0.01), and TNF-alpha (p<0.01) expressions elevated by I/R injury. Furthermore, visnagin reversed I/R induced M1/M2 macrophage polarization (CD86 up arrow, CD163 down arrow), decreasing CD86 (p<0.05) and increasing CD163 immunodensity (p<0.05). Conclusions: Visnagin treatment (60 mg/kg) exerts promising nephroprotective effects in renal I/R injury by reducing oxidative stress, inflammation, apoptosis, and modulating M1/M2 macrophage polarization.
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; Ozoner, M. Pekince
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.