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    18β-glycyrrhetinic acid Mitigates bisphenol A-induced liver and renal damage: Inhibition of TNF-α/NF-κB/p38-MAPK, JAK1/STAT1 pathways, oxidative stress and apoptosis
    (Elsevier Ltd, 2025) Darendelioğlu, Ekrem; Cağlayan, Cüneyt; Küçükler, Sefa; Bayav, İbrahim; Kandemir, Fatih Mehmet; Ayna, Adnan; Sağ, Sevda
    Bisphenol A (BPA) has been commonly used in various consumer products, including water bottles, food containers, and canned food linings. However, there are concerns about its potential toxicity to human health, particularly its impact on the liver and kidneys. The objective of this research was to investigate the potential ameliorative effects of 18β-glycyrrhetinic acid (GA) against BPA-induced hepatotoxicity and nephrotoxicity in rats. The animals were supplemented with BPA (250 mg/kg b.w.) alone or with GA (50 and 100 mg/kg b.w.) for 14 days. GA treatment alleviated the BPA-induced hepato-renal tissue injuries through reducing the serum ALT, AST and ALP levels, and urea and creatinine levels. GA co-treatment also increased activities of SOD, CAT and GPx enzymes and levels of GSH, and suppressed MDA levels in BPA induced tissues. BPA also induced inflammation by increasing the levels of TNF-α, NF-κB, JAK1, STAT1, P38 MAPK and JNK in liver and kidney tissues and GA treatment ameliorated these effects. BPA triggered apoptosis by increasing caspase-3, Bax, and cytochrome c at protein levels and also by decreasing the antiapoptotic Bcl-2 level. However, treatment with GA (50 and 100 mg/kg) decreased apoptosis. Overall, our results have revealed the potential ameliorative mechanisms of GA, as a possible agent for BPA-induced hepatotoxicity and nephrotoxicity.
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    Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats
    (Springer Science and Business Media B.V., 2023) Varışlı, Behçet; Çağlayan, Cüneyt; Kandemir, Fatih Mehmet; Gür, Cihan; Ayna, Adnan; Ayna, Adnan; Genç, Aydın; Taysı, Seyithan
    Diclofenac (DF) is a non-steroidal anti-inflammatory drug (NSAID) generally prescribed for the treatment of pain. In spite of the widespread use of DF, hepatotoxicity has been reported after its administration. The current study discloses new evidence as regards of the curative effects of chrysin (CHR) on DF-induced hepatotoxicity by regulating oxidative stress, apoptosis, autophagy, and endoplasmic reticulum (ER) stress. Methods: The animals were separated into five different groups. Group-I was in control. Group-II received CHR-only (50 mg/kg bw, p.o.) on all 5 days. Group-III received DF-only (50 mg/kg bw, i.p.) on 4th and 5th day. Group-IV received DF (50 mg/kg bw) + CHR (25 mg/kg, bw) and group-V received DF (50 mg/kg, bw) + CHR (50 mg/kg, bw) for 5 days. Results: DF injection was associated with increased MDA while reduced GSH level, activities of superoxide dismutase, glutathione peroxidase, and catalase and mRNA levels of HO-1 and Nrf2 in the liver. DF injection caused apoptosis and autophagy in the liver by up-regulating caspase-3, Bax, LC3A, and LC3B levels and down-regulating Bcl-2. DF also caused ER stress by increasing mRNA transcript levels of ATF-6, IRE1, PERK, and GRP78. Additionally, it was observed that DF administration up-regulated MMP2 and MMP9. However, treatment with CHR at a dose of 25 and 50 mg/kg considerably ameliorated oxidative stress, apoptosis, autophagy, and ER stress in liver tissue. Conclusion: Overall, the data of this study indicate that liver damage associated with DF toxicity could be ameliorated by CHR administration.
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    Hesperidin attenuates oxidative stress, inflammation, apoptosis, and cardiac dysfunction in sodium fluoride?Induced cardiotoxicity in rats
    (Springer, 2022) Varışlı, Behçet; Darendelioğlu, Ekrem; Çağlayan, Cüneyt; Kandemir, Fatih Mehmet; Ayna, Adnan; Genç, Aydın; Kandemir, Özge
    Excessive fluoride intake has been reported to cause toxicities to brain, thyroid, kidney, liver and testis tissues. Hesperidin (HSP) is an antioxidant that possesses anti-allergenic, anti-carcinogenic, anti-oxidant and anti-inflammatory activities. Presently, the studies focusing on the toxic effects of sodium fluoride (NaF) on heart tissue at biochemical and molecular level are limited. This study was designed to evaluate the ameliorative effects of HSP on toxicity of NaF on the heart of rats in vivo by observing the alterations in oxidative injury markers (MDA, SOD, CAT, GPX and GSH), pro-inflammatory markers (NF-?B, IL-1?, TNF-?), expressions of apoptotic genes (caspase-3, -6, -9, Bax, Bcl-2, p53, cytochrome c), levels of autophagic markers (Beclin 1, LC3A, LC3B), expression levels of PI3K/Akt/mTOR and cardiac markers. HSP treatment attenuated the NaF-induced heart tissue injury by increasing activities of SOD, CAT and GPx and levels of GSH, and suppressing lipid peroxidation. In addition, HSP reversed the changes in expression of apoptotic (caspase-3, -6, -9, Bax, Bcl-2, p53, cytochrome c), levels of autophagic and inflammatory parameters (Beclin 1, LC3A, LC3B, NF-?B, IL-1?, TNF-?), in the NaF-induced cardiotoxicity. HSP also modulated the gene expression levels of PI3K/Akt/mTOR signaling pathway and levels of cardiac markers (LDH, CK-MB). Overall, these findings reveal that HSP treatment can be used for the treatment of NaF-induced cardiotoxicity.
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    Morin ameliorates methotrexate-induced hepatotoxicity via targeting Nrf2/HO-1 and Bax/Bcl2/Caspase-3 signaling pathways
    (Springer, 2023) Kızıl, Hamit Emre; Çağlayan, Cüneyt; Darandelioğlu, Ekrem; Ayna, Adnan; Gür, Cihan; Kandemir, Fatih Mehmet; Küçükler, Sefa
    Organ toxicity limits the therapeutic efficacy of methotrexate (MTX), an anti-metabolite therapeutic that is frequently used as an anti-cancer and immunosuppressive medicine. Hepatocellular toxicity is among the most severe side effects of long-term MTX use. The present study unveils new confirmations as regards the remedial effects of morin on MTX-induced hepatocellular injury through regulation of oxidative stress, apoptosis and MAPK signaling.
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    Neuroprotective effects of 18 beta-glycyrrhetinic acid against bisphenol A-induced neurotoxicity in rats: involvement of neuronal apoptosis, endoplasmic reticulum stress and JAK1/STAT1 signaling pathway
    (Springer, 2022) Çağlayan, Cüneyt; Kandemir, Fatih Mehmet; Ayna, Adnan; Gür, Cihan; Küçükler, Sefa; Darendelioğlu, Ekrem
    The exposure to bisphenol A (BPA) is inevitable owing to its common use in the production of polycarbonate plastics. Studies to reduce side effects are gaining importance since BPA causes severe toxicities in important tissues such as testes, lungs, brain, liver and kidney. The current study was planned to study ameliorative effect of 18 beta-glycyrrhetinic acid (18 beta-GA) on BPA induced neurotoxicity. Fourty Wistar albino rats were divided into five equal groups as follows: I-Control group, II-18 beta-GA group (100 mg/kg), III- BPA group (250 mg/kg), IV-250 mg/kg BPA +50 mg/kg 18 beta-GA group, V-250 mg/kg BPA +100 mg/kg 18 beta-GA group. BPA intoxication was associated with increased MDA level while reduced GSH concentration, activities of glutathione peroxidase, superoxide dismutase, and catalase. BPA supplementation caused apoptosis in the brain by up-regulating caspase-3 and Bax levels and down-regulating Bcl-2. BPA also caused endoplasmic reticulum (ER) stress by increasing mRNA transcript levels of PERK, IRE1, ATF-6 and GRP78. Additionally, it was observed that BPA administration activated JAK1/STAT1 signaling pathway and levels of TNF-alpha, NF-kappa B, p38 MAPK and INK in the brain. However, co-treatment with 18 beta-GA at a dose of 50 and 100 mg/kg considerably ameliorated oxidative stress, inflammation, apoptosis, ER stress and JAK1/STAT1 signaling pathway in brain tissue. Overall, the data of this study indicate that brain damage associated with BPA toxicity could be ameliorated by 18 beta-GA administration.