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Öğe Hesperidin ameliorates vancomycin-induced kidney injury via multipathway modulation: Nrf-2/HO-1, Caspase-3/Bax/Bcl-2, ATF-4, KIM-1 and improved renal tissue function(Elsevier Inc., 2025) Gencer, Selman; Şimşek, Hasan; Akaras, Nurhan; Gür, Cihan; İleritürk, Mustafa; Kandemir, Özge; Küçükler, Sefa; Kankılıç, Nazım Abdülkadir; Kandemir, Fatih MehmetVancomycin (VCM) is a therapeutic agent used to treat drug-resistant gram-positive bacteria. However, its high-dose use is associated with nephrotoxicity, limiting its clinical application. Hesperidin (HES), a flavonoid naturally found in citrus fruits, exhibits various biological and pharmacological activities, including anti-inflammatory, antioxidant, and anticancer effects. While HES has been shown to exert protective effects in several organ systems, its potential role in preventing VCM-induced nephrotoxicity remains unclear. This study investigates whether HES can mitigate VCM-induced renal damage through its antioxidant and anti-inflammatory properties. VCM was administered intraperitoneally at a dose of 200 mg/kg for seven days. HES (100 mg/kg and 200 mg/kg) was administered orally for seven days. Biochemical, and molecular methods were used to investigate indicators of oxidative stress, ER stress damage, apoptotic and autophagic death in kidney tissue. Additionally, histological methods were used to determine the structural and functional characteristics of kidney tissue. HES treatment alleviated VCM-induced oxidative stress by increasing antioxidants (SOD, CAT, GPx, GSH) and reducing increased MDA levels, a marker of lipid peroxidation. In addition, HES increased antioxidant activity by activating the Nrf2 signaling pathway. VCM-induced increases in apoptotic Bax, Caspase-3, and P53 were reduced by HES, while the decreased level of antiapoptotic Bcl-2 was increased. HES reduced VCM-induced ER stress damage by reducing the levels of ATF-4, ATF-6, eIF2-α, and CHOP. HES treatment attempted to preserve kidney function and structural integrity. Overall, HES was effective in reducing VCM-induced nephrotoxicity damage and may be an effective treatment option.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.Öğe The Protective Effects of Chrysin on Acrylamide-Induced Hepatotoxicity: Insights Into Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histological Evaluation in Rats(John Wiley and Sons Inc, 2025) Gencer, Selman; Akaras, Nurhan; Şimşek, Hasan; Gür, Cihan; İleritürk, Mustafa; Küçükler, Sefa; Kandemir, Fatih MehmetAcrylamide (ACR) is a toxic chemical with a high carcinogenic risk that is released as a result of heating or processing foods at high temperatures. Chrysin (CHR) is a flavonoid that is naturally found in foods such as honey and passionflower and stands out with its antioxidant, anticancer, and anti-inflammatory properties. This study aims to determine the protective effects of CHR in ACR-induced hepatotoxicity. ACR was administered orally at a dose of 38.27 mg/kg; CHR (25 or 50 mg/kg) was administered orally for ten days. Biochemical and molecular methods were used to investigate oxidative stress, inflammation, and apoptotic markers in liver tissue. Additionally, histological methods were used to determine the liver tissue's structural and functional characteristics and autophagy. CHR treatment alleviated ACR-induced oxidative stress by increasing antioxidants (SOD, CAT, GPx, GSH) and reducing increased oxidant MDA. CHR reduced inflammatory activity by inactivating NF-κB and pro-inflammatory cytokines. ACR-induced increases in apoptotic Casp-3, Casp-6, Casp-9, and Bax were reduced by CHR, while the decreased level of antiapoptotic Bcl-2 was increased. It was also determined immunohistochemically that CHR inhibited autophagic Beclin-1 activity. CHR was effective in reducing ACR-induced hepatotoxicity damage and may be an effective treatment option.Öğe Therapeutic potential of rosmarinic acid in tramadol-induced hepatorenal toxicity: Modulation of oxidative stress, inflammation, RAGE/NLRP3, ER stress, apoptosis, and tissue functions parameters(Elsevier Ltd, 2025) Karaca, Onur; Akaras, Nurhan; Şimşek, Hasan; İleritürk, Mustafa; Küçükler, Sefa; Gencer, Selman; Kandemir, Fatih MehmetTramadol (TRM), a widely used opioid analgesic for moderate to severe pain, is associated with liver and kidney toxicity at high doses or prolonged use. This study investigates the protective role of rosmarinic acid (RA), a natural phenolic compound known for its antioxidant, anti-inflammatory, and cell-protective properties, against TRM-induced hepatorenal toxicity. Methods: Thirty-five male Wistar rats were divided into five groups: Control, TRM, RA, TRM + RA25, and TRM + RA50. Rats received TRM (50 mg/kg) and RA (25 or 50 mg/kg), with liver and kidney function tests, oxidative stress, inflammation, ER stress, apoptosis, and tissue damage indicators assessed through qRT-PCR, ELISA, Western blotting, H&E, and immunohistochemical analysis. Results: TRM induced liver and kidney dysfunctions, evident from increased ALT, AST, ALP, urea, creatinine, nephrin, TIM-1 and 8-OHdG levels, along with activated oxidative stress, inflammation, ER stress, and apoptosis pathways. RA significantly reduced these effects, ameliorating histologic and immunohistochemical markers of tissue damage and inflammation. Conclusion: RA demonstrates therapeutic potential by mitigating TRM-induced hepatorenal toxicity and preserving tissue integrity.
