Sürdürülebilir Kalkınma Amaçları
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- MakaleYalnız künye2021Scopus SJRQ1Protective Effects of Chrysin Against Oxidative Stress and Inflammation Induced by Lead Acetate in Rat Kidneys: a Biochemical and Histopathological Approach
Kucukler, Sefa; Benzer, Fulya; Yildirim, Serkan; Gur, Cihan; Kandemir, Fatih Mehmet; Bengu, Aydin Sukru; Ayna, Adnan; Caglayan, Cuneyt; Dortbudak, Muhammet Bahaeddin
In this study, the protective effects of chrysin (CR) on lead acetate (PbAc)-induced renal toxicity in Sprague-Dawley rats were investigated with biochemical, histopathological, and immunohistochemical methods. In the study, rats were given orally at 30 mg/kg/body weight (BW) PbAc after CR of 25 and 50 mg/kg/BW was administered to them orally (a total of 7 administrations for 7 days). The results showed that CR reduced urea and creatinine levels by alleviating PbAc-induced kidney damage. It was determined that CR decreases PbAc-induced lipid peroxidation due to its antioxidant properties and increases catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and glutathione (GSH) levels. It was also detected that CR protects DNA from the toxic effects of PbAc and reduces 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels. Biochemical and immunohistochemical findings demonstrated that CR had anti-inflammatory and antiapoptotic effects and reduced nuclear factor kappa-B (NF-κB), interleukin-33 (IL-33), prostaglandin-E2 (PGE-2), tumor necrosis factor-α (TNF-α), p53 levels, and the activities of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), which were increased with PbAc administration. Moreover, CR was found to increase the levels of aquaporin-1 (AQP-1) and nephrine in PbAc-induced kidney tissue. CR decreased the contents of lead (Pb), zinc (Zn), iron (Fe), sodium (Na), and copper (Cu) and increased those of potassium (K) calcium (Ca) in renal tissue. These results indicated that CR considerably alleviates kidney toxicity caused by PbAc.
AtıfScopus136WoS118OpenAlex145İncele
- MakaleYalnız künye2018Scopus SJRQ2Chemoprotective effects of curcumin on doxorubicin-induced nephrotoxicity in wistar rats: by modulating inflammatory cytokines, apoptosis, oxidative stress and oxidative DNA damage
Benzer, Fulya; Kandemir, Fatih Mehmet; Kucukler, Sefa; Comaklı, Selim; Caglayan, Cuneyt
Doxorubicin (DXR) is one of the most important chemotherapeutic agent. However, nephrotoxicity reduces its clinical utility in humans. The aim of the study was to investigate protective effects of curcumin (CMN) against DXR-induced nephrotoxicity. Rats were subjected to oral treatment of CMN (100 and 200 mg/kg body weight) for 7 days. Nephrotoxicity was induced by single intra peritoneal injection of DXR (40 mg/kg body weight) on the fifth day and then the experiment was terminated on the eighth day. Nephroprotective effects of CMN were associated with decrease in serum toxicity markers and increase in antioxidant enzyme activities. CMN was able to reduced the levels of inflammatory markers such as TNF-α, NF-κB, IL-1β, iNOS and COX-2 in the rats. It also reduced the expressions of apoptotic marker including caspase-3, and oxidative DNA damage marker including 8-OHdG. Collectively, these findings indicated that CMN protect against DXR-induced nephrotoxicity.
AtıfScopus116WoS111OpenAlex122İncele
- MakaleYalnız künye2018Scopus SJRQ3Curcumin ameliorates doxorubicin-induced cardiotoxicity by abrogation of inflammation, apoptosis, oxidative DNA damage, and protein oxidation in rats
Benzer, Fulya; Kandemir, Fatih Mehmet; Ozkaraca, Mustafa; Kucukler, Sefa; Caglayan, Cuneyt
Doxorubicin (DXR) is a highly effective drug for chemotherapy. However, cardiotoxicity reduces its clinical utility in humans. The present study aimed to assess the ameliorative effect of curcumin against DXR-induced cardiotoxicity in rats. Rats were subjected to oral treatment of curcumin (100 and 200 mg/kg body weight) for 7 days. Cardiotoxicity was induced by single intraperitoneal injection of DXR (40 mg/kg body weight) on the 5th day and the rats sacrificed on 8th day. Curcumin ameliorated DXR-induced lipid peroxidation, glutathione depletion, decrease in antioxidant (superoxide dismutase, catalase, and glutathione peroxidase) enzyme activities, and cardiac toxicity markers (CK-MB, LDH, and cTn-I). Curcumin also attenuated activities of Caspase-3, cyclooxygenase-2, inducible nitric oxide synthase, and levels of nuclear factor kappa-B, tumor necrosis factor-α, and interleukin-1β, and cardiac tissue damages that were induced by DXR. Moreover, curcumin decreased the expression of 8-OHdG and 3,3′-dityrosine. This study demonstrated that curcumin has a multi-cardioprotective effect due to its antioxidant, anti-inflammatory, and antiapoptotic properties.
AtıfScopus154WoS143OpenAlex163İncele

