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Öğe Increased triglyceride-glucose index predicts contrast-induced nephropathy in non-diabetic NSTEMI patients: A prospective study(SAGE Publications Inc., 2023) Aktaş, Halil; İnci, Sinan; Gül, Murat; Gencer, Selman; Yıldırım, OğuzThe triglyceride-glucose (TyG) index is a new reliable marker of insulin resistance (IR) and has recently been reported to be associated with renal dysfunction and contrast-induced nephropathy (CIN). Our aim in this study is to investigate the relationship between the TyG index and CIN in non-diabetic non-ST elevation acute myocardial infarction (NSTEMI) patients. The study included 272 non-diabetic patients who applied with NSTEMI and underwent coronary angiography (CAG). Patient data were divided into quartiles according to the TyG index: Q1: TyG??9.29. Baseline characteristics, laboratory measurements, angiography data, and the incidence of CIN were compared between the groups. CIN was observed in 18 (6.6%) patients in the study. The incidence of CIN was lowest in the Q1 group and highest in the Q4 group (1 (1.5%) in Q1; 3 (4.4%) in Q2; 5 (7.4%) in Q3; 9 (13.2%) in Q4; p?=?0.040). TyG index was found to be an independent risk factor for the development of CIN in multivariate logistic regression analysis (odds ratio?=?6.58; confidence interval (CI)?=?2.12–20.40; p?=?0.001). TyG index value of 9.17 was identified as an effective cut-off point for the prediction of CIN (Area under the curve: 0.712, CI: 0.590–0.834, p?=?0.003), and it had a sensitivity of 61% and a specificity of 72%. The results of this study showed that a high TyG index increases the incidence of CIN after CAG in non-diabetic NSTEMI patients and is an independent risk factor for the development of CIN.Öğe The ameliorative effect of carvacrol on sodium arsenite-induced hepatotoxicity in rats: Possible role of Nrf2/HO-1, RAGE/NLRP3, Bax/Bcl-2/Caspase-3, and Beclin-1 pathways(John Wiley and Sons Inc, 2024) Gencer, Selman; Gür, Cihan; İleritürk, Mustafa; Küçükler, Sefa; Akaras, Nurhan; Şimşek, Hasan; Kandemir, Fatih M.Arsenic is a toxic environmental pollutant heavy metal, and one of its critical target tissues in the body is the liver. Carvacrol is a natural phytocompound that stands out with its antioxidant, anti-inflammatory, and antiapoptotic properties. The current study aims to investigate the protective feature of carvacrol against sodium arsenite-induced liver toxicity. Thirty-five Sprague-Dawley male rats were divided into five groups: Control, Sodium arsenite (SA), CRV, SA + CRV25, and SA + CRV50. Sodium arsenite was administered via oral gavage at a dose of 10 mg/kg for 14 days, and 30 min later, CRV 25 or 50 mg/kg was administered via oral gavage. Oxidative stress, inflammation, apoptosis, autophagy damage pathways parameters, and liver tissue integrity were analyzed using biochemical, molecular, western blot, histological, and immunohistological methods. Carvacrol decreased sodium arsenite-induced oxidative stress by suppressing malondialdehyde levels and increasing superoxide dismutase, catalase, glutathione peroxidase activities, and glutathione levels. Carvacrol reduced inflammation damage by reducing sodium arsenite-induced increased levels of NF-?B and the cytokines (TNF-?, IL-1?, IL-6, RAGE, and NLRP3) it stimulates. Carvacrol also reduced sodium arsenite-induced autophagic (Beclin-1, LC3A, and LC3B) and apoptotic (P53, Apaf-1, Casp-3, Casp-6, Casp-9, and Bax) parameters. Carvacrol preserved sodium arsenite-induced impaired liver tissue structure. Carvacrol alleviated toxic damage by reducing sodium arsenite-induced increases in oxidative stress, inflammation, apoptosis, and autophagic damage parameters in rat liver tissues. Carvacrol was also beneficial in preserving liver tissue integrity.Öğe The ameliorative effect of carvacrol on sodium arsenite‐ induced hepatotoxicity in rats: Possible role of Nrf2/HO‐1, RAGE/NLRP3, Bax/Bcl‐2/Caspase‐3, and Beclin‐1 pathways(Wiley, 2024) Gencer, Selman; Gür, Cihan; İleritürk, Mustafa; Küçükler, Sefa; Akaras, Nurhan; Şimşek, Hasan; Kandemir, Fatih M.Arsenic is a toxic environmental pollutant heavy metal, and one of its critical target tissues in the body is the liver. Carvacrol is a natural phytocompound that stands out with its antioxidant, anti‐inflammatory, and antiapoptotic properties. The current study aims to investigate the protective feature of carvacrol against sodium arsenite‐ induced liver toxicity. Thirty‐five Sprague‐Dawley male rats were divided into five groups: Control, Sodium arsenite (SA), CRV, SA + CRV25, and SA + CRV50. Sodium arsenite was administered via oral gavage at a dose of 10 mg/kg for 14 days, and 30 min later, CRV 25 or 50 mg/kg was administered via oral gavage. Oxidative stress, inflammation, apoptosis, autophagy damage pathways parameters, and liver tissue integrity were analyzed using biochemical, molecular, western blot, histological, and immunohistological methods. Carvacrol decreased sodium arsenite‐induced oxidative stress by suppressing malondialdehyde levels and increasing superoxide dismutase, catalase, glutathione peroxidase activities, and glutathione levels. Carvacrol reduced inflammation damage by reducing sodium arsenite‐induced increased levels of NF‐κB and the cytokines (TNF‐α, IL‐1β, IL‐6, RAGE, and NLRP3) it stimulates. Carvacrol also reduced sodium arsenite‐induced autophagic (Beclin‐1, LC3A, and LC3B) and apoptotic (P53, Apaf‐1, Casp‐3, Casp‐6, Casp‐9, and Bax) parameters. Carvacrol preserved sodium arsenite‐induced impaired liver tissue structure. Carvacrol alleviated toxic damage by reducing sodium arsenite‐induced increases in oxidative stress, inflammation, apoptosis, and autophagic damage parameters in rat liver tissues. Carvacrol was also beneficial in preserving liver tissue integrity.Öğe The ameliorative effects of chrysin on bortezomib-induced nephrotoxicity in rats: Reduces oxidative stress, endoplasmic reticulum stress, inflammation damage, apoptotic and autophagic death(Elsevier Ltd, 2024) Kankılıç, Nazım Abdülkadir; Şimşek, Hasan; Akaras, Nurhan; Gür, Cihan; Küçükler, Sefa; Gencer, Selman; Kandemir, Fatih MehmetBortezomib is a proteasome inhibitor antineoplastic agent that was the first to be approved for cancer treatment. One of bortezomib's most prominent dose-limiting effects is nephrotoxicity; the underlying mechanism is believed to be oxidative stress. Chrysin is a compound found actively in honey and many plant species and stands out with its antioxidant properties. The present study aimed to determine the ameliorative effects of chrysin in bortezomib-induced nephrotoxicity. Material-method: Thirty-five male Wistar rats were divided into control, BTZ, CHR, BTZ + CHR25, and BTZ + CHR50. Biochemical, molecular, Western blot, and histological methods analyzed renal function indicators, oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and damage pathways. Results: Chrysin decreased oxidative stress by reducing oxidants (MDA) and increasing antioxidants (SOD, CAT, Gpx, GSH, Nrf-2, HO-1, NQO1). Chrysin reduced endoplasmic reticulum stress by decreasing ATF-6, PERK, IRE1, and GRP-78 levels. Chrysin reduced inflammation damage by inhibiting the NF-?B pathway. Chrysin exhibited protective properties against apoptotic damage by decreasing Bax and Caspase-3 levels and increasing Bcl-2 levels. In addition, chrysin improved renal function and structural integrity and exhibited healing properties against toxic damage in tissue structure. Conclusion: Overall, chrysin exhibited an ameliorative effect against bortezomib-induced nephrotoxicity.
