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Biol Trace Elem Res ; 2020 Jun 29.
Artigo em Inglês | MEDLINE | ID: mdl-32613487


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.

Food Chem Toxicol ; 138: 111190, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32068001


Acrylamide (ACR) is a heat-induced carcinogen substance that is found in some foods due to cooking or other thermal processes. The aim of present study was to assess the probable protective effects of morin against ACR-induced hepatorenal toxicity in rats. The rats were treated with ACR (38.27 mg/kg b.w., p.o.) alone or with morin (50 and 100 mg/kg b.w., p.o.) for 10 consecutive days. Morin treatment attenuated the ACR-induced liver and kidney tissue injury by diminishing the serum AST, ALP, ALT, urea and creatinine levels. Morin increased activities of SOD, CAT and GPx and levels of GSH, and suppressed lipid peroxidation in ACR induced tissues. Histopathological changes and immunohistochemical expressions of p53, EGFR, nephrin and AQP2 in the ACR-induced liver and kidney tissues were decreased after administration of morin. In addition, morin reversed the changes in levels of apoptotic, autophagic and inflammatory parameters such as caspase-3, bax, bcl-2, cytochrome c, beclin-1, LC3A, LC3B, p38α MAPK, NF-κB, IL-1ß, IL-6, TNF-α and COX-2 in the ACR-induced toxicity. Morin also affected the protein levels by regulating the PI3K/Akt/mTOR signaling pathway and thus alleviated ACR-induced apoptosis and autophagy. Overall, these findings may shed some lights on new approaches for the treatment of ACR-induced hepatotoxicity and nephrotoxicity.

J Trace Elem Med Biol ; 56: 60-68, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31442956


OBJECTIVE: Mercury is a global environmental pollutant and is responsible for several organ pathophysiology including oxidative stress-induced liver disorders. Therefore, the present study was conducted to evaluate the potential ameliorative effects of rutin on mercury chloride (HgCl2)-induced hepatotoxicity in adult male rats. METHODS: HgCl2 was intraperitoneally injected at a dose of 1.23 mg/kg body weight for 7 days alone or in combination with the orally rutin (50 and 100 mg/kg body weight). RESULTS: Rutin treatment significantly improved liver function tests [alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT)], and increased activities of antioxidant defense system [catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)] and glutathione (GSH) content. The histological alterations and epidermal growth factor receptor (EGFR) expression in the HgCl2-induced liver tissues were decreased by administration of rutin. Furthermore, rutin reversed the changes in levels of apoptosis and inflammation related proteins involving p53, Bcl-2 associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), cytochrome c, nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), B-cell lymphoma-3(Bcl-3) and interleukin-1ß (IL-1ß), and inhibited p38α mitogen-activated protein kinase (MAPK) and cysteine aspartate specific protease-3 (caspase-3) activations. CONCLUSION: The data of the present study suggest that rutin effectively suppress HgCl2-induced hepatotoxicity by ameliorating oxidative stress, inflammation and apoptosis.

Apoptose/efeitos dos fármacos , Inflamação/patologia , Fígado/patologia , Cloreto de Mercúrio/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Rutina/uso terapêutico , Animais , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/uso terapêutico , Antioxidantes/metabolismo , Biomarcadores/sangue , Receptores ErbB/metabolismo , Glutationa/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/enzimologia , Fígado/lesões , Masculino , Ratos Sprague-Dawley , Rutina/química , Rutina/farmacologia , Proteína Supressora de Tumor p53/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
Chem Biol Interact ; 308: 89-100, 2019 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-31100273


Although Doxorubicin (DOX) is a widespread drug used in the treatment of cancer, its clinical use is restricted due to its common side effects. In addition, administrating DOX with an antioxidant has recently become a new strategy in preventing the side effects of DOX. The protective effects of morin, a natural flavonoid, against DOX-induced liver and kidney damage in rats were investigated biochemically, immunohistochemically and histopathologically in this study. The experimental procedure was planned as 10 days, and 5 groups consisting of seven rats were formed. Morin was given orally to rats at a dose of 50 and 100 mg/kg for 10 days and DOX was given a single dose of 40 mg/kg intraperitoneally on day 8. In order to determine the protective effect of morin against oxidative stress caused by DOX, reduced glutathione (GSH) and malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) enzyme activities were measured in liver and kidney tissues. Liver and kidney tissue damage were determined both histopathologically and by serum alanine transaminase (ALT), aspartate transaminase (AST), urea and creatinine analysis. In order to determine the effect of DOX-induced inflammation and against the effect of morin, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and nuclear factor kappa B (NF-κB) levels were determined in both tissues. Liver and kidney B-cell lymphoma-2 (Bcl-2) levels were determined biochemically. In addition, Bax expression in liver tissue and aquaporin-2 (AQP-2) and nephrin expression in renal tissue were determined immunohistochemically. It was determined that oxidative damage caused by DOX decreased and improvement of liver and kidney function markers were observed in the groups that were treated with morin. In addition, pre-treatment of morin showed a regulatory effect on TNF-α, IL-1ß and NF-κB levels. It prevented the increase in DOX-induced Bax expression and decrease in Bcl-2 level, AQP-2 and nephrin expression. Histopathological examination revealed that it prevented tissue damage in liver and kidney tissues.

Doxorrubicina/toxicidade , Flavonoides/farmacologia , Fígado/efeitos dos fármacos , Substâncias Protetoras/farmacologia , Alanina Transaminase/sangue , Animais , Antioxidantes/metabolismo , Aquaporina 2/metabolismo , Aspartato Aminotransferases/sangue , Glutationa/metabolismo , Rim/efeitos dos fármacos , Rim/metabolismo , Rim/patologia , Fígado/metabolismo , Fígado/patologia , Masculino , Proteínas de Membrana/metabolismo , NF-kappa B/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo
BMC Vet Res ; 14(1): 406, 2018 Dec 18.
Artigo em Inglês | MEDLINE | ID: mdl-30563529


BACKGROUND: Even though gas gangrene caused by Clostridium septicum in goats is mentioned in the classical textbooks, we have not managed to find any case description in the literature. CASE PRESENTATION: Clinical signs resembling gas gangrene such as subcutaneous bloating, edema and crepitation were detected at various body parts of nine pregnant animals at the ages of 2-3 years on a hair goat farm (n = 170) located in Bingol province, Eastern Turkey. Five of these suspected animals with severe clinical symptoms died within 2 days. Various samples such as internal organs, edematous skin and edema fluid collected from dead and live animals were analyzed for the presence of clostridial agents by histopathological and microbiological methods. As a result of macroscopic and microscopic examination, lesions of gas gangrene were detected. The suspected isolates were identified and confirmed as C. septicum by bacteriological and molecular methods. CONCLUSION: The present study was the first to report identification of C. septicum as primary agent in the gas gangrene of goats.

Clostridium septicum , Morte Súbita/etiologia , Morte Súbita/veterinária , Gangrena Gasosa/veterinária , Doenças das Cabras/microbiologia , Animais , Feminino , Gangrena Gasosa/complicações , Gangrena Gasosa/diagnóstico , Gangrena Gasosa/microbiologia , Doenças das Cabras/diagnóstico , Cabras , Turquia
Biomed Pharmacother ; 105: 981-991, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30021393


Vancomycin (VCM) is a glycopeptidic broad-spectrum antibiotic against methicillin-resistant Staphylococcus aureus, though it has some adverse effects, including nephrotoxicity, that limit its usefulness. Zingerone (ZO), a component of dry ginger root, has several pharmacological activities due to its antioxidant, anti-inflammatory and antiapoptotic properties. The aim of this study was to determine the therapeutic efficacy of ZO against VCM-induced oxidative stress, inflammation, apoptosis and kidney aquaporin 1 (AQP1) levels in rats. Intraperitoneal administration of VCM (200 mg/kg body weight) for seven days increased kidney lipid peroxidation and decreased antioxidant enzyme activities, including kidney superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). VCM increased serum creatinine and urea levels and induced histopathological changes while causing a decrease in AQP1 protein level. VCM also increased the levels of the inflammatory markers nuclear factor kappa B (NF-κB), B-cell lymphoma-3(Bcl-3), interleukin-1ß (IL-1ß), interleukin-33 (IL-33), tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), myeloperoxidase (MPO) and cyclooxygenase-2 (COX-2). Moreover, it activated the apoptotic pathway by increasing the expression levels of p53, Bcl-2 associated X protein (Bax), cysteine aspartate specific protease-3 (caspase-3) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), which is a marker of oxidative DNA damage. Treatment with ZO (25 and 50 mg/kg body weight) at both doses prevented nephrotoxicity by ameliorating the histopathological alterations, oxidative stress, inflammation, apoptosis, oxidative DNA damage and renal AQP1 levels. The findings of the present study suggested that ZO attenuates VCM-induced nephrotoxicity.

Apoptose/efeitos dos fármacos , Aquaporina 1/antagonistas & inibidores , Guaiacol/análogos & derivados , Rim/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Vancomicina/toxicidade , Animais , Antibacterianos/toxicidade , Apoptose/fisiologia , Aquaporina 1/metabolismo , Guaiacol/farmacologia , Guaiacol/uso terapêutico , Inflamação/induzido quimicamente , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Rim/metabolismo , Masculino , Staphylococcus aureus Resistente à Meticilina/efeitos dos fármacos , Estresse Oxidativo/fisiologia , Permeabilidade/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Resultado do Tratamento