Browsing by Author "Tekiner, Deniz"

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Astaxanthin-Loaded Silver Nanoparticles Mitigate 6-Ohda Parkinson's Via Er Stress and Pi3k/Akt Signaling
(Springer, 2025) Kara, Hulya; Tekiner, Deniz; Ustundag, Hilal; Bayram, Cemil; Sebin, Saime Ozbek; Ozkanlar, Seckin; Kara, Adem
Parkinson's disease (PD) is characterized by progressive dopaminergic neuronal loss, with oxidative stress and neuroinflammation as critical pathological mechanisms. The blood-brain barrier presents a significant challenge for therapeutic delivery, while current treatments provide only symptomatic relief without halting disease progression. This study investigated the neuroprotective effects of astaxanthin-loaded citrate-coated silver nanoparticles (AST-AgNPs), leveraging their potent antioxidant properties, anti-inflammatory capacity, and enhanced blood-brain barrier penetration. In vitro cytotoxicity analyses were performed using 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y neuroblastoma cells, while in vivo experiments utilized a unilateral 6-OHDA-induced rat model. Following 14 days of treatment, comprehensive evaluations included behavioral assessments, biochemical analyses (MDA, GSH, SOD, TNF-alpha, IL-1 beta, IFN-gamma), histopathology, immunohistochemistry (BrdU, tyrosine hydroxylase), and molecular analyses. Western blot measured CHOP, IRE1, ATF6, p-AKT, total AKT, caspase-3, and cleaved caspase-3, while RT-PCR quantified caspase-3, Bcl-2, Bax, PI3K, mTOR, Akt, CREB, and NF-kappa B-p65 expression. AST-AgNP treatment significantly ameliorated motor dysfunction, reduced neuroinflammation (TNF-alpha, IL-1 beta), improved oxidative stress parameters (MDA, GSH, SOD), and preserved dopaminergic neurons (all p < 0.05). Western blot revealed significant downregulation of ER stress markers (CHOP, IRE1, ATF6) and cleaved caspase-3, while restoring p-AKT and total AKT levels (p < 0.05). RT-PCR demonstrated decreased pro-apoptotic gene expression (caspase-3, NF-kappa B-p65) and increased anti-apoptotic Bcl-2 expression (p < 0.05). These findings demonstrate that AST-AgNPs provide neuroprotection through simultaneous modulation of ER stress and PI3K/Akt/mTOR pathways, representing a novel dual-pathway therapeutic strategy for PD addressing multiple pathological mechanisms through enhanced nanoparticle-mediated delivery.
Effects of Silver Nanoparticle-Loaded 18β-Glycyrrhetinic Acid on P2x7 Receptor and Endoplasmic Reticulum Stress-Mediated Nlrp3 Inflammasome Activation in Testicular Tissue in an Animal Diabetes Model
(Wiley, 2025) Gelen, Volkan; Yesildag, Ali; Akarsu, Serkan Ali; Kara, Hulya; Tekiner, Deniz; Kara, Adem
Diabetes, a metabolic disease characterized by high blood sugar, causes damage to many organs in the body. Accordingly, the present study investigates the effects of silver nanoparticle-loaded 18 beta-glycyrrhetinic acid (AgNP+18 beta-GA) on P2X7 receptor and ER stress-mediated NLRP3 inflammasome activation in testicular tissue. 42 Wistar-Albino rats aged 6 months were used. The rats were divided into the following seven groups: Control, AgNP+18 beta-GA100, DM, DM-18 beta-GA100, DM-AgNP+18 beta-GA50, DM-AgNP+18 beta-GA100, and DM-AgNP. After the experiment, sperm samples obtained from the rats were evaluated. Oxidative stress markers, serum IL-1 beta, and TNF-alpha levels were determined in the testicular tissue samples taken separately. In addition, Caspase-1, NLRP3, P2X7, Caspase-3, NF-kappa B, IRE1, ATF6, and CHOP protein expression levels were evaluated using Western blot analysis of histopathological examinations. Specifically, the most significant decrease was observed in NLRP3, Caspase-1, P2X7, and NF-kappa B levels in the DM-AgNP+18 beta-GA100 group (p < 0.05). About sperm parameters, while sperm motility and viability significantly decreased in diabetic groups (p < 0.05), a significant improvement in these values was observed in the AgNP+18 beta-GA applied groups (p < 0.05). AgNP+18 beta-GA improved sperm morphology and histopathological damage in diabetes-induced testicular damage, as well as inhibited P2X7 receptor and endoplasmic reticulum stress-mediated NLRP3 inflammasome activation.