The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury

Keşim, Dilek Aygün; Aşır, Fırat; Ayaz, Hayat; Korak, Tuğcan

doi:10.3390/cimb46020102

Cited by 3 publications

(1 citation statement)

References 63 publications

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“…The reactions were stopped using a PBS solution, and the sections were counterstained with hematoxylin dye. Subsequently, the slides were mounted and imaged using a Zeiss Imager A2 light microscope [29].…”

Section: Immunohistochemical Examinationmentioning

confidence: 99%

Zonisamide Ameliorated the Apoptosis and Inflammation in Cerebellar Tissue of Induced Alcohol Addiction Animal Model

Aşır,

Erdemci,

Çankırı

et al. 2024

Life

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This study investigated the effects of zonisamide treatment on cerebellar tissues in an experimental alcohol addiction (AA) model and its potential mechanisms of action, particularly regarding apoptotic protease activating factor-1 (APAF-1) and tumor necrosis factor-alpha (TNF-α) expression. Thirty rats were divided into three groups: sham, ethanol (EtOH), and EtOH + zonisamide. AA was induced by administering 6 cc of EtOH orally every 8 h for 4 days. Zonisamide (100 mg/kg) was given to rats once daily before EtOH administration. Motor defects were evaluated using an open field maze. Serum TNF-α levels were measured from blood samples. Cerebellar sections were processed for histological examination and immunostained for APAF-1 and TNF-α. Protein interaction networks were constructed using Cytoscape, and functional annotations were performed with ShinyGO (version 0.80) software. The traveled area in the EtOH group was significantly reduced compared to the sham group (p = 0.0005). Rats in the EtOH + zonisamide group covered a larger area, with zonisamide treatment significantly improving locomotor ability compared to the EtOH group (p = 0.0463). Serum TNF-α levels were significantly elevated in the EtOH group compared to the sham group (p < 0.0001) and were significantly decreased in the EtOH + zonisamide group compared to the EtOH group (p = 0.0309). Regular cerebellar histological layers were observed in the sham group, while EtOH induction caused loss of cerebellar tissue integrity, neuronal degeneration, vascular dilatation and congestion, reduced myelin density, and neuropils in the EtOH group. Zonisamide treatment improved these pathologies, enhancing myelination and neuropil formation. Negative APAF-1 and TNF-α expressions were observed across cerebellar layers in the sham group. Due to EtOH toxicity, APAF-1 and TNF-α expression were upregulated in the EtOH group compared to the sham group (p < 0.001 for both). Zonisamide treatment downregulated these protein expressions in the EtOH + zonisamide group compared to the EtOH group (p < 0.001 and p = 0.0087, respectively). APAF-1 was primarily associated with AA through antifolate resistance, endopeptidases, and the interleukin-1 pathway, while TNF-α was predominantly enriched in infections and choline-binding, indicating zonisamide’s impact on immune and inflammatory pathways. In conclusion, zonisamide treatment significantly mitigated ethanol-induced cerebellar damage and inflammation in an AA model. Zonisamide improved locomotor function and reduced serum TNF-α levels, as well as APAF-1 and TNF-α expression in cerebellar tissues. These findings suggest that zonisamide exerts its protective effects by modulating immune and inflammatory pathways, thereby preserving cerebellar integrity and function.

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Section: Immunohistochemical Examinationmentioning

confidence: 99%

Zonisamide Ameliorated the Apoptosis and Inflammation in Cerebellar Tissue of Induced Alcohol Addiction Animal Model

Aşır,

Erdemci,

Çankırı

et al. 2024

Life

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CITED1 expression in odontogenic cysts

Aşır,

Özalp,

Yülek

et al. 2024

BMC Oral Health

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Background Originating from odontogenic tissue, Odontogenic cysts are pathological cavities lined with epithelial cells and surrounded by fibrous connective tissue. This study investigated expression of CITED1 protein in different types of odontogenic cysts. Material and method 40 keratocysts, 40 radicular cysts, and 40 dentigerous cysts were excised and processed for routine paraffin wax embedding protocol. Macroscopic and panoramic radiographies images were used for diagnosis. Demographical properties and dental parameters were recorded. Cystic tissues were stained with hematoxylin-eosin dye and CITED1 antibody. Semi-quantitative analysis was performed for immune staining. The protein-protein interaction network, hub gene detection and KEGG analysis were conducted using Cytoscape software. Result Odontogenic keratocysts was imaged with 6–8 layered epithelial cells and fibrous cyst walls with inflammatory cells. Radicular cysts had stratified squamous epithelium with varying thickness, ciliated cells, and Rushton hyaline bodies. Dentigerous cysts presented hyperplastic non-keratinized epithelium, fibrous tissue, rete ridges, and inflammatory cells. CITED1 immunoexpression was highest in odontogenic keratocysts, followed by radicular cysts, and lowest in dentigerous cysts. Nuclear and cytoplasmic CITED1 expression was significantly elevated in odontogenic keratocysts compared to radicular and dentigerous cysts. The top five targets of CITED1 were identified, primarily showing enrichment in hormone and cancer related pathways. Conclusions Positive CITED1 expression in all three types of odontogenic cysts suggest a potential role for CITED1 in the pathogenesis of odontogenic cysts, particularly in keratocysts. Further investigations are needed to elucidate the exact mechanisms underlying the differential expression of CITED1 and its implications for the development and progression of odontogenic cysts.

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Skimmianine Showed Neuroprotection against Cerebral Ischemia/Reperfusion Injury

Ayaz,

Aşır,

Korak

2024

CIMB

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The aim of this study was to investigate the antioxidant and anti-inflammatory effects of skimmianine on cerebral ischemia–reperfusion (IR) injury. Twenty-four female Wistar albino rats were randomly divided into three groups: Sham, Ischemia–Reperfusion (IR), and IR + Skimmianine (40 mg/kg Skimmianine). Cerebral ischemia was induced using a monofilament nylon suture to occlude the middle cerebral artery for 60 min. Following 23 h of reperfusion, the animals were sacrificed 14 days later. The effects of skimmianine on brain tissue post-IR injury were examined through biochemical and immunochemical analyses. In silico analysis using the Enrichr platform explored skimmianine’s potential biological processes involving IBA-1, IL-6, and NF-κB proteins. In the IR group, MDA levels increased, while SOD and CAT antioxidant enzyme activities decreased. In the IR + Skimmianine group, skimmianine treatment resulted in decreased MDA levels and increased SOD and CAT activities. Significant increases in IBA-1 expression were observed in the IR group, which skimmianine treatment significantly reduced, modulating microglial activation. High levels of IL-6 expression were noted in pyramidal neurons, vascular structures, and neuroglial cells in the IR group; skimmianine treatment reduced IL-6 expression, demonstrating anti-inflammatory effects. Increased NF-κB expression was observed in neurons and blood vessels in the gray and white matter in the IR group; skimmianine treatment reduced NF-κB expression. Gene Ontology results suggest skimmianine impacts immune and inflammatory responses via IBA-1 and IL-6, with potential effects on estrogen mechanisms mediated by NF-κB. Skimmianine may be a potential therapeutic strategy due to its antioxidant and anti-inflammatory effects on cerebral IR injury.

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The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury

Cited by 3 publications

References 63 publications

Zonisamide Ameliorated the Apoptosis and Inflammation in Cerebellar Tissue of Induced Alcohol Addiction Animal Model

Zonisamide Ameliorated the Apoptosis and Inflammation in Cerebellar Tissue of Induced Alcohol Addiction Animal Model

CITED1 expression in odontogenic cysts

Skimmianine Showed Neuroprotection against Cerebral Ischemia/Reperfusion Injury

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