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BACKGROUND: Hexavalent chromium (CrVI) is known to be a potentially hepatotoxic and nephrotoxic contaminant in humans and other animals, whose toxicity is associated with oxidative stress and inflammation. The aim of this study was to evaluate the potential protective effect of chlorogenic acid (CGA), which has known anti-inflammatory and antioxidant effects, on potassium dichromate (PDC)-induced acute hepatotoxicity and nephrotoxicity in rats. METHODS AND RESULTS: Thirty-six Wistar albino rats were treated with CGA (10, 20, or 40 mg/kg, intraperitoneally) and/or PDC (15 mg/kg/day, intraperitoneally) as a single dose. Serum, liver, and kidney tissues were examined biochemically, histopathologically, and immunohistochemically. Compared to the control group, a significant increase in interleukin-6 (IL-6) levels and a significant decrease in serum and renal reduced glutathione (GSH) levels, liver catalase (CAT), tumour necrosis factor-alpha (TNF-α), and interleukin 1ß (IL-1ß) levels were observed in the PDC group. The administration of PDC led to histopathological and immunohistochemical changes in rat liver and kidney tissues. With the administration of CGA, especially at the 10 mg/kg dosage, the above-mentioned parameters approached normal levels. CONCLUSIONS: CGA had antioxidant and anti-inflammatory effects that alleviated PDC-induced acute hepato- and nephrotoxicity.
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Antioxidantes , Ácido Clorogênico , Rim , Fígado , NF-kappa B , Estresse Oxidativo , Dicromato de Potássio , Ratos Wistar , Transdução de Sinais , Animais , Dicromato de Potássio/toxicidade , Ácido Clorogênico/farmacologia , Ratos , Transdução de Sinais/efeitos dos fármacos , NF-kappa B/metabolismo , Rim/efeitos dos fármacos , Rim/metabolismo , Rim/patologia , Estresse Oxidativo/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Masculino , Antioxidantes/farmacologia , Antioxidantes/metabolismo , Interleucina-6/metabolismo , Glutationa/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Interleucina-1beta/metabolismo , Catalase/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológicoRESUMO
The most prominent adverse effects of nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac (DF) are hepato-renal damage. Natural antioxidants can be preferred as an alternative and/or combination to improve this damage. This present study was conducted to evaluate the protective effect of Tubuloside A (TA) against diclofenac (DF)-induced hepato-renal damage. TA (1 mg/kg, ip) was administered to male Sprague-Dawley rats for 5 days, and DF (50 mg/kg, ip) was administered on Days 4 and 5. Plasma aspartate amino transferase, alanine amino transferase, alkaline phosphatase, blood urea nitrogen and creatinine were measured to evaluate liver and kidney functions. Additionally, oxidative stress parameters (malondialdehyde, glutathione, superoxide dismutase, catalase, and 8-oxo-7,8-dihydro-2'-deoxyguanosine) in blood, liver, and kidney tissues, changes in mRNA expression of genes involved in the Nrf2/HO-1 signalling pathway (Nrf2, HO-1, NQO-1, IL-6, iNOS, Cox-2, TNF-α, IL1-ß and NFκB) and apoptotic process (Bcl-2, Cas-3 and Bax) in liver and kidney tissues were determined. Additionally, tissue sections were evaluated histopathologically. Biochemical, histopathological, and molecular results demonstrated the hepato-renal toxic effects of DF, and TA treatment protected the liver and kidney from DF-induced damage. This provides an explanation for the hepato-nephro damage caused by DF and offers new ideas and drug targets together with TA for the prevention and treatment of DF injury.
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Diclofenaco , Fator 2 Relacionado a NF-E2 , Ratos , Animais , Masculino , Diclofenaco/farmacologia , Diclofenaco/metabolismo , Fator 2 Relacionado a NF-E2/genética , Fator 2 Relacionado a NF-E2/metabolismo , Glicosídeos/farmacologia , Ratos Sprague-Dawley , Estresse Oxidativo , Antioxidantes/farmacologia , Antioxidantes/metabolismo , Rim/patologia , ApoptoseRESUMO
BACKGROUND: Neurological disorders result in not only a decline in the quality of life of patients but also a global economic burden. Therefore, protective medicine becomes more important for society. MK-801 is a chemical agent used to understand the etiology of behavioral disorders and brain degeneration in animal models. This study aims to determine whether N-acetylcysteine (NAC) is useful to treat brain degeneration caused by MK-801, an N-methyl-D-aspartate glutamate receptor antagonist. METHODS AND RESULTS: Four groups were formed by dividing 24 male BALB/c mice into groups of six. The control group was given a saline solution (10 ml/kg-i.p.). MK-801 (1 mg/kg-i.p.) was given alone to one group, and it was given with NAC (100 mg/kg-i.p.) to another group, while the last group was given only NAC (100 mg/kg-i.p.). The administration of drugs lasted for fourteen days. After the behavioral tests (open field and elevated plus-maze), all animals were euthanised, and brain tissues were collected for real-time PCR, TAS-TOS analysis, hematoxylin-eosin, Kluver-Barrera, and TUNEL staining. In the MK-801 group, besides nuclear shrinkage in neurons, glial cell infiltration, vacuolization in cortical neurons, white matter damage, and apoptosis were observed. CONCLUSION: In the mice given NAC as a protective agent, it was observed that behavioral problems improved, antioxidant levels increased, and nuclear shrinkage, glial cell infiltration, vacuolization in neurons, and white matter degeneration were prevented. Moreover, MBP expression increased, and the number of TUNEL-positive cells significantly decreased. As a result, it was observed that NAC may have a protective effect against brain degeneration.
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Acetilcisteína , Maleato de Dizocilpina , Humanos , Camundongos , Animais , Masculino , Acetilcisteína/farmacologia , Maleato de Dizocilpina/farmacologia , Qualidade de Vida , Antioxidantes/farmacologia , Antagonistas de Aminoácidos Excitatórios , Substâncias ProtetorasRESUMO
Favipiravir is a nucleoside analogue antiviral drug and inhibits the replication of many RNA viruses, especially influenza viruses. Favipiravir has also been used to treat patients with mild to moderate COVID-19 disease. However, various side effects, including neurological side effects, have been reported related to the use of favipiravir. Therefore, in this study, we aimed to investigate the possible effects of favipiravir alone or in combination with vitamin C on aged rats' brain tissue and the possible mechanisms of these effects. A total of 30 rats used in the study were randomly divided into 5 equal groups and the first group was kept as the control group. High-dose (100 mg/kg) or low-dose (20 mg/kg) favipiravir was administered alone or in combination with vitamin C (150 mg/kg) to other groups. Administration of both high and low doses of favipiravir significantly increased TBARS levels in brain tissue of aged rats. Similarly, both high and low doses of favipiravir led to significant increases in Bcl-2 and caspase-3 relative mRNA expression. However, only low dose favipiravir caused a significant increase in iNOS and IL-1ß relative mRNA expression levels. Similar results were also observed in histopathological examinations. However, co-administration of vitamin C with favipiravir attenuated some of the adverse effects of favipiravir. In conclusion, in this study, it was shown that the use of favipiravir caused some adverse effects through oxidative, inflammatory and apoptotic processes in the brain tissue of aged rats, and the potential of vitamin C to alleviate these effects.
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Background: Favipiravir (FPV), an effective antiviral agent, is a drug used to treat influenza and COVID-19 by inhibiting the RNA-dependent RNA polymerase (RdRp) of RNA viruses. FPV has the potential to increase oxidative stress and organ damage. The purpose of this study was to demonstrate the oxidative stress and inflammation caused by FPV in the liver and kidneys of rats, as well as to investigate the curative effects of vitamin C (VitC).Methods: A total of 40 Sprague-Dawley male rats were randomly and equally divided into the following five groups: 1st; Control, 2nd; FPV = 20 mg/kg, 3rd; FPV = 100 mg/kg, 4th; FPV = 20 mg/kg + VitC (150 mg/kg), and 5th; FPV = 100 mg/kg + VitC (150 mg/kg) groups. Rats were given either FPV (orally) or FPV plus VitC (intramuscular) for 14 days. Rat blood, liver, and kidney samples were collected at 15 days to be analyzed for oxidative and histological changes.Results: FPV administration resulted in an increase in proinflammatory cytokines (TNF-α and IL-6) in the liver and kidney, as well as oxidative and histopathologic damage. FPV increased TBARS levels significantly (p < .05) and decreased GSH and CAT levels in liver and kidney tissues but had no effect on SOD activity. VitC supplementation significantly reduced TNF-a, IL-6, and TBARS levels while increasing GSH and CAT levels (p < .05). Furthermore, VitC significantly attenuated FPV-induced histopathological alterations associated with oxidative stress and inflammation in the liver and kidney tissues (p < .05).Conclusion: FPV caused liver and kidney damage in rats. In contrast, co-administration of FPV with VitC improved FPV-induced oxidative, pro-inflammatory, and histopathological changes.
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COVID-19 , Interleucina-6 , Ratos , Masculino , Animais , Interleucina-6/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Ratos Sprague-Dawley , COVID-19/metabolismo , Estresse Oxidativo , Ácido Ascórbico/farmacologia , Ácido Ascórbico/metabolismo , Ácido Ascórbico/uso terapêutico , Antioxidantes/farmacologia , Antioxidantes/metabolismo , Fígado , Rim , Inflamação/induzido quimicamente , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Suplementos NutricionaisRESUMO
BACKGROUND: Fecal incontinence (FI) generally occurs with anal sphincter damage caused by vaginal delivery in women, obvious FI can develop in the postmenopausal stage. This pelvic floor dysfunction has no rational medical therapeutic options. We investigated the effect of testosterone treatment on the anal sphincter structure, serum thiol/disulfide levels, uterine tissue, and body composition in female rats in an experimental menopause-FI model. METHODS: The animal experiments were performed between September and November 2020 at Experimental Animal Application and Research Center, Afyon Kocatepe University, Afyonkarahisar, Turkey. Thirty-two female rats were divided into four groups: sham, saline, 10 mg/kg testosterone undecanoate, 100 mg/kg testosterone undecanoate. Except for the sham group, all the other groups underwent ovariectomy (OVE) to create a menopause model. Two weeks after this procedure, the FI model was created under general anesthesia in all rat groups. At the end of the experiment, the rats were placed under general anesthesia, weighed, and euthanized after recording the data. The anal sphincter region and uterine tissue samples were collected for histopathological examinations, and blood samples were collected for total testosterone and thiol/disulfide homeostasis analyses. RESULTS: An increase in anal sphincter muscles and connective tissue thickness was observed in the testosterone-administered groups (p = 0.001). No difference was detected between the groups in the total thiol, native thiol, and disulfide balance (p = 0.087, p = 0.604, p = 0.092). The testosterone-treated groups did not have severe uterine epithelial degradation, hyperemia, or increased endometrial thickness (p = 0.186, p = 0.222, p = 0.630). The body weight of all rats increased (p < 0.05), but the omental weight did not increase (p = 0.061). DISCUSSION: Testosterone treatment increased the anal sphincter muscle and connective tissue thickness without causing any oxidative stress and did not result in a pathological change in the uterine tissue and body fat composition.
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Canal Anal , Incontinência Fecal , Gravidez , Feminino , Animais , Ratos , Incontinência Fecal/tratamento farmacológico , Parto Obstétrico/efeitos adversos , Músculo Liso , Testosterona/farmacologiaRESUMO
Background/aim: Ischemia-reperfusion (IR) injury to a part of the body can cause damage to distant organs such as the kidney and heart. This study investigated the protective effects of safranal against IR-induced renal injury. Materials and methods: Used in this study were 24 Wistar Albino male rats, which were divided into 3 equal and randomised groups. The sham group underwent laparotomy only. In the IR group, the infrarenal aorta was clamped for 1 h, and then reperfused for 2 h. In the IR-safranal group, safranal was administered 30 min before the procedure and IR injury was induced in the same way as in the IR group. After the procedure, blood and tissue samples were collected from the rats for biochemical and histopathological analyses. Antioxidant capacity and proinflammatory cytokine analyses were performed on the blood samples. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was performed to determine the number of cells undergoing apoptosis in the kidney tissue. Results: The estimated glomerular filtration rate, an indicator of renal function, was lower in the IR group (p1 = 0.024 vs. p3 = 0.041, respectively) compared to the other groups, while creatinine levels were higher in the IR group compared to the other groups (p1 = 0.032 vs. p2 = 0.044, respectively). The blood urea nitrogen level was higher in the IR group than in the other groups (p1 = 0.001vs p2 = 0.035, respectively). The total antioxidant and total oxidant status, indicating tissue oxidative stress, did not differ between groups (p = 0.914 vs. p = 0.184, respectively). Among the proinflammatory cytokines, the interleukin-1ß (IL-1ß) and IL-6 levels were significantly higher in the IR group (p = 0.034 vs. p = 0.001, respectively), but the tumour necrosis factor-α (p = 0.19), and interferon-γ (p = 0.311) levels did not differ between groups. Histopathological examination showed significantly less damage to glomerular and tubular cells in the IR-safranal group (p < 0.001). The number of TUNEL-positive cells was higher in the IR group compared to the other groups (p < 0.001). Conclusion: Safranal may have protective effects against kidney damage caused by distant ischemia-reperfusion injury.
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Cicloexenos , Rim , Ratos Wistar , Traumatismo por Reperfusão , Animais , Traumatismo por Reperfusão/prevenção & controle , Masculino , Ratos , Rim/patologia , Rim/efeitos dos fármacos , Cicloexenos/farmacologia , Modelos Animais de Doenças , Apoptose/efeitos dos fármacos , Aorta Abdominal/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Terpenos/farmacologia , Antioxidantes/farmacologiaRESUMO
The aim of the present study was to investigate the possible protective effects of boron, an antioxidant agent, against arsenic-induced oxidative stress in male and female rats. In total, 42 Wistar albino male and female rats were divided into three equal groups: The animals in the control group were given normal drinking water, the second group was given drinking water with 100 mg/L arsenic, and the third group was orally administered drinking water with 100 mg/kg boron together with arsenic. At the end of the 28-day experiment, arsenic increased lipid peroxidation and damage in the tissues of rats. However, boron treatment reversed this arsenic-induced lipid peroxidation and activities of antioxidant enzymes in rats. Moreover, boron exhibited a protective action against arsenic-induced histopathological changes in the tissues of rats. In conclusion, boron was found to be effective in protecting rats against arsenic-induced lipid peroxidation by enhancing antioxidant defense mechanisms.
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Antioxidantes/metabolismo , Arsênio/toxicidade , Boro/farmacologia , Peroxidação de Lipídeos/efeitos dos fármacos , Animais , Peso Corporal/efeitos dos fármacos , Catalase/metabolismo , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Comportamento Alimentar/efeitos dos fármacos , Feminino , Glutationa/metabolismo , Hemoglobinas/metabolismo , Masculino , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismoRESUMO
Organophosphorus compounds cause oxidative stress and lead to alterations in antioxidant status in organisms. In this study, the effects of subchronic exposure to malathion and the protective effects of boron (B) were evaluated in 48 Wistar rats, which were divided equally into six groups. For 28 d, the control group received a normal diet and tap water, the corn oil group received a normal diet and 0.5 mL of corn oil by gastric gavage and the malathion group received a normal diet and malathion (100 mg/kg/d) by gastric gavage. During the same period, each of the three other groups received a different dosage of B (5, 10 and 20 mg/kg/d, respectively) and malathion (100 mg/kg/d) by gastric gavage. Malathion administration during the period increased malondialdehyde, nitric oxide and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, as well as markers of liver function, yet decreased acetylcholinesterase, reduced glutathione, superoxide dismutase, and catalase activities in blood, liver, kidney and brain tissues. Administration of B in a dose-dependent manner also reversed malathion-induced oxidative stress, lipid peroxidation (LPO) and antioxidant enzyme activity. Moreover, B exhibited protective action against malathion-induced histopathological changes in liver, kidney and brain tissues. These results demonstrate that, if used in a dose-dependent manner, B decreases malathion-induced oxidative stress, enhances the antioxidant defense mechanism and regenerates tissues in rats.
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Antioxidantes/metabolismo , Boro/farmacologia , Malation/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Acetilcolinesterase/efeitos dos fármacos , Acetilcolinesterase/metabolismo , Animais , Boro/administração & dosagem , Encéfalo/efeitos dos fármacos , Encéfalo/patologia , Relação Dose-Resposta a Droga , Glutationa/metabolismo , Rim/efeitos dos fármacos , Rim/patologia , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/patologia , Masculino , Malondialdeído/metabolismo , Óxido Nítrico/metabolismo , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismoRESUMO
Wound healing is a complex process and one of the major therapeutic and economic subjects in the pharmaceutical area. In recent years, the fabrication of nano-sized wound dressing models has attracted great attention for tissue regeneration. Plant extracts loaded nanoparticles are environmentally friendly and non-toxic and the release of the bioactive substance will be controlled to the wound area. This study aims to fabricate wound dressing models that contain bioactive components for tissue regeneration. Fungal chitosan/polycaprolactone nanofiber was fabricated by electrospinning and it has been characterized. Plant extracts loaded nanoliposomes were prepared, characterized, and embedded in nanofiber structures. The effectiveness of wound dressing models for tissue regeneration was evaluated by in vitro and in vivo studies. It was observed that all wound dressing models positively affect the cell viability of human dermal fibroblast cells. It was determined that plant extracts loaded nanoparticles embedded in nanofibers increased in cell viability than nanoparticles that were non-embedded in nanofiber structures. Histological analysis showed that plant extract-loaded nanoliposomes embedded in chitosan/PCL nanofibers were used for tissue regeneration. The most effective nanofibers were determined as Wd-ClNL nanofibers. RESEARCH HIGHLIGHTS: Hypericum perforatum L. and Cistus laurifolius L. were prepared by modified ultrasonic extraction method. Fungal chitosan/polycaprolactone nanofiber was fabricated by electrospinning and it has been characterized. Plant extract-loaded nanoliposomes were prepared, and characterized. They were embedded in chitosan/polycaprolactone nanofiber. Effects of the wound dressing model were analyzed by in vitro and in vivo assays for tissue regeneration.
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Quitosana , Nanofibras , Poliésteres , Humanos , Quitosana/química , Nanofibras/química , Cicatrização , Extratos Vegetais/farmacologia , Bandagens , Antibacterianos/farmacologiaRESUMO
Pyraclostrobin, a strobilurin-derived fungicide, causes oxidative stress and DNA damage in the organism. Taurine plays an important role in metabolic processes such as osmoregulatory, cytoprotective, and antioxidant effects. The study aimed to investigate the protective effect of taurine in Sprague Dawley male rats exposed to pyraclostrobin. The rats were separated into 6 groups and were found 8 animals in each group. Rats were given 30 mg/kg pyraclostrobin and pyraclostrobin together with three different taurine concentrations (50, 100, and 200 mg/kg) via oral gavage for 28 days. While pyraclostrobin increased biochemical parameters, lipid peroxidation, and DNA damage, it decreased glutathione levels and enzyme activities of catalase and superoxide dismutase. Pyraclostrobin increased apoptotic, proinflammatory, and CYP2E1 mRNA expression levels, whereas antiapoptotic gene Bcl-2 mRNA expression levels decreased in liver tissue. Additionally, pyraclostrobin caused histopathological alterations in tissues. Taurine in a dose-dependent manner reversed the changes caused by pyraclostrobin. As a result, taurine exhibited a cytoprotective effect by showing antioxidant, anti-inflammatory, and antiapoptotic activities against oxidative damage caused by pyraclostrobin.
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It is seen that cyclophosphamide, which is used in treating many diseases, especially cancer, causes toxicity in studies, and its metabolites induce oxidative stress. This study aimed to investigate the protective effects of resveratrol and Coenzyme Q10, known for their antioxidant properties, separately and together, against oxidative stress induced by cyclophosphamide. In this study, 35 Wistar albino male rats were divided into five groups. Groups; Control group, cyclophosphamide (CP) group (CP as 75 mg kg i.p. on day 14), coenzyme Q10 (CoQ10) + CP group (20 mg/kg i.p. CoQ10 + 75 mg kg i.p. CP), resveratrol (Res) + CP group (20 mg/kg i.p. Res + 75 mg/kg i.p. CP), CoQ10 + Res + CP group (20 mg/kg i.p Res + 20 mg/kg i.p CoQ10 and 75 mg/kg i.p.CP). At the end of the experiment, the cholesterol, creatinine and urea levels of the group given CP increased, while a decrease was observed in the groups given Res and CoQ10. Malondialdehyde level was high, glutathione level, superoxide dismutase and catalase activities were decreased in the blood and all tissues (liver, kidney, brain, heart and testis) of the CP given group. DNA damage and histopathological changes were also observed. In contrast, Res and CoQ10, both separately and together, reversed the CP-induced altered level and enzyme activities and ameliorated DNA damage and histopathological changes. In this study, the effects of Res and CoQ10 against CP toxicity were examined both separately and together.
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OBJECTIVES: In this study, we aimed to determine the bioefficacy of epidermal growth factor (EGF), boric acid (BA), and their combination on cartilage injury in rats. MATERIALS AND METHODS: In in vitro setting, the cytotoxic effects of BA, EGF, and their combinations using mouse fibroblast cell (L929), human bone osteosarcoma cell (Saos-2), and human adipose derived mesenchymal stem cells (hAD-MSCs) were determined by applying MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] test. In in vivo setting, 72 rats were randomly divided into four groups. A standard chondral defect was created and microfracture was performed in all groups. Group A was determined as the control group. In addition to the standard procedure, Group B received 100 ng/mL of EGF, Group C received a combination of 100 ng/mL of EGF and 10 µg/mL of BA combination, and Group D 20 µg/mL of BA. RESULTS: The cytotoxic effect of the combinations of EGF dilutions (1, 5, 10, 25, 50, 100, 200 ng/mL) with BA (100, 300, 500 µg/mL) was observed only in the 72-h application period and in Saos-2. The cytotoxic effect of BA was reduced when combined with EGF. There was no significant difference in the histopathological scores among the groups (p=0.13). CONCLUSION: Our study showed that EGF and low-dose BA application had a positive effect on cartilage healing in rats. Significant decreases in recovery scores were observed in the other groups. The combination of EGF and BA promoted osteoblast growth. Detection of lytic lesions in the group treated with 20 µg/mL of BA indicates that BA may have a cytotoxic effect.
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Ácidos Bóricos , Cartilagem , Fator de Crescimento Epidérmico , Animais , Humanos , Camundongos , Ratos , Ácidos Bóricos/farmacologia , Ácidos Bóricos/uso terapêutico , Cartilagem/efeitos dos fármacos , Cartilagem/lesões , Fator de Crescimento Epidérmico/farmacologia , Fator de Crescimento Epidérmico/uso terapêutico , Fator de Crescimento Epidérmico/metabolismo , Linhagem CelularRESUMO
In the present study, we investigated the protective effect of magnolin (MAG) against oxidative stress induced by cyclophosphamide (CP) and its role in the Nrf2/HO-1 signaling pathway. Rats were administered MAG (1 mg/kg, i.p.) for 14 days and CP (75 mg/kg, i.p.) on the 14th day. CP administration increased tissue damage, as evidenced by elevated levels of transaminases (aspartate and alanine), alkaline phosphatase, and renal parameters (blood urea nitrogen and creatinine). Additionally, 8-hydroxy-2'-deoxyguanosine and malondialdehyde levels were increased, whereas glutathione levels, along with catalase and superoxide dismutase activities, decreased in CP-treated rats. CP also down-regulated the expression of Bcl-2, HO-1, Nrf2, and NQO-1, while up-regulating Bax, Cas-3, TNF-α, Cox-2, iNOS, IL-6, IL-1ß, and NFκB in liver and kidney tissues. In addition, CP treatment caused histopathological changes in heart, lung, liver, kidney, brain, and testis tissues. Treatment with MAG improved biochemical and oxidative stress parameters and prevented histopathological changes in CP-treated rats. Moreover, MAG suppressed the expression of inflammatory cytokines and apoptosis markers. In conclusion, MAG effectively prevented CP-induced toxicity by reducing oxidative stress, inflammation, and apoptosis, with its protective efficacy associated with the up-regulation of Nrf2/HO-1 signaling.
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The aim of this study was to clarify the effects of dietary supplementation with Yucca schidigera (Ys) on lipid peroxidation (LPO), antioxidant activity, some biochemical parameters and histopathological changes in arsenic-exposed mice. Forty Swiss albino male mice were divided into five equal groups. Group I (control group) was given normal diet and tap water for 28 days. Group II (arsenic group) was given normal diet and 100 mg/L arsenic along with drinking water for 28 days. Groups III-V were given three different doses of Ys (50, 100 and 200 mg/kg) in supplemented diet and arsenic (100 mg/L) along with drinking water throughout the entire period of 28 days. The arsenic significantly increased serum biochemical parameters and malondialdehyde levels in blood and tissue. However, arsenic significantly decreased tissue glutathione concentration, erythrocyte superoxide dismutase and catalase activities. In contrast, dietary supplementation of Ys, in a dose-dependent manner, resulted in reversal of arsenic-induced oxidative stress, LPO and activities of antioxidant enzymes. Moreover, Ys also exhibited protective action against the arsenic-induced focal gliosis and hyperemi in brain, necrosis and degeneration in liver, degeneration and dilatation in Bowman's capsule of kidney and hyaline degeneration in heart tissue of mice. Consequently, our results demonstrate that Ys especially high-dose supplementation in diet decreases arsenic-induced oxidative stress and enhances the antioxidant defence mechanism and regenerate of tissues in Swiss albino mice.
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Arsênio/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Preparações de Plantas/farmacologia , Yucca/química , Animais , Peso Corporal/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Encéfalo/patologia , Glutationa/análise , Glutationa/sangue , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/química , Fígado/efeitos dos fármacos , Fígado/patologia , Masculino , Camundongos , Especificidade de Órgãos , Oxirredutases/sangueRESUMO
We aimed to evaluate the effects of postpartum progesterone on obstetric anal sphincter injury (OASI) healing in female rats using an experimental OASI model. Twenty-eight female rats were divided into four groups after birth: sham-30, sham-90, progesterone (P4)-30, and P4-90. Moreover, OASI model was established in all groups. Subsequently, except for the sham groups, medroxyprogesterone acetate (0.15 mg) was intramuscularly injected into the P4 groups. After 30 and 90 days, the rats were euthanized under general anesthesia after recording the data. The anal sphincter region was collected for histopathological examination. Progesterone and thiol/disulfide homeostasis studies were performed on blood samples. No significant differences were observed between the groups regarding the external anal sphincter (EAS), internal anal sphincter (IAS), or connective tissue thickness (p = 0.714, p = 0.135, and p = 0.314, respectively). No statistically significant differences in the total thiol, native thiol, disulfide, and progesterone levels were found between the groups (p = 0.917, p = 0.503, p = 0.361, and p = 0.294, respectively). The endometrial thickness was lower in the P4 groups than in the sham groups (p = 0.031). Postpartum progesterone administration did not affect IAS and EAS or connective tissue thickness or disrupt the thiol-disulfide balance. However, this administration led to endometrial thinning.
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Acetaminophen (APAP) is one of the popular and safe pain medications worldwide. However, due its wide availability, it is frequently implicated in intentional or unintentional overdoses where it can cause severe liver injury and even acute liver failure. Boron is a bioactive trace element, found naturally as boric acid (BA) and borate. In this study, the effects of boric acid on the acute renal toxicity induced by APAP in rats were researched in comparison with N-acetyl cysteine (NAC). In the study, 7 groups were formed and 2 g/kg dose of paracetamol per rat was prepared by suspending in 1% Carboxy Methyl Cellulose (CMC) solution of phosphate buffer saline (PBS). Boric acid dissolved in saline was administered to experimental animals by gavage at doses of 50, 100, and 200 mg/kg. In this study, ER stress and apoptosis formed by paracetamol-induced nephrotoxicity were investigated. This purpose determined iNOS, PERK, ATF6, NFkB p53, caspases 3, 12, bcl-2, and bcl-xL gene mRNA expression kidney tissue. Also, the levels of kidney injury molecule-1 (KIM-1), Cysteine (Cys), and IL-18 levels, which are mentioned today as kidney damage markers were compared with BUN and creatine levels. The effect of boron on kidney damage was determined by histopathologic. Data were statistically analyzed by using SPSS-20 ANOVA and stated as means and standard deviation. According to the data obtained in our study, we believe that boric acid has a protective effect on the negative effects of paracetamol on the kidney. We believe that our study will provide useful data to the literature on the possibility of a supplement to be used as an active compound in paracetamol for the prophylaxis of boric acid and it can also be converted into a useful product.
Assuntos
Acetaminofen , Nefropatias , Ratos , Animais , Acetaminofen/toxicidade , Acetaminofen/metabolismo , Boro/farmacologia , Acetilcisteína/farmacologia , Apoptose , Nefropatias/induzido quimicamente , Estresse do Retículo EndoplasmáticoRESUMO
BACKGROUND: Aflatoxins are one of the important environmental factors that pose a risk to living organisms. On the other hand, it has been indicated in research that boron intake has beneficial effects on organisms. In this study, the effect of boron was disclosed in rats exposed to aflatoxin B1 (AFB1), which poses a toxicological risk. METHODS: A total of 36 male Sprague Dawley rats were separated into 6 groups and 0.125 mg/kg bw AFB1 and 5, 10, or 20 mg/kg bw doses of boron were given orally for 21 days. End of the experiment, biochemical, molecular, and histopathological analyses were performed. RESULTS: AFB1 treatment increased liver enzyme activities (AST, ALT, and ALP) and malondialdehyde level; on the other hand, it caused a decrease in glutathione level, superoxide dismutase and catalase activities. In addition, the mRNA expression levels of apoptotic (Bax, Caspase-3, Caspase-8, Caspase-9, and p53) and pro-inflammatory (TNF-α and NFκB) genes increased and the mRNA expression of the anti-apoptotic gene (Bcl-2) decreased in liver tissue. Also, AFB1 treatment increased DNA damage and caused histopathological alterations in the liver tissue. Additionally, boron applications at doses of 5, 10, and 20 mg/kg bw given with AFB1 reversed these negative changes. CONCLUSIONS: As a result, boron exhibited hepatoprotective effect together with antioxidant, anti-inflammatory, and anti-apoptotic effects against AFB1-induced liver damage.
Assuntos
Aflatoxina B1 , Antioxidantes , Ratos , Masculino , Animais , Antioxidantes/farmacologia , Antioxidantes/metabolismo , Aflatoxina B1/toxicidade , Aflatoxina B1/metabolismo , Boro/farmacologia , Boro/metabolismo , Ratos Sprague-Dawley , Estresse Oxidativo , Anti-Inflamatórios/farmacologia , Fígado/metabolismo , RNA Mensageiro/metabolismoRESUMO
2,4-dichlorophenoxyacetic acid (2,4-D) and arsenic cause severe and extensive biological toxicity in organisms. However, their interactions and toxic mechanisms in co-exposure remain to be fully elucidated. In this study, 28 four-week-old female rats were divided into four groups and exposed to 100 mg/L arsenic or/and 600 mg/L 2,4-D through drinking water for a period of 28 days. As a result, it was revealed that biochemical indicators (ALT, AST, ALP, blood urea nitrogen, and creatinine) were increased and decreased hormonal parameters (FSH, LH, PG, and E2) in arsenic and 2,4-D and arsenic combination-treated groups. Moreover, increased lipid peroxidation (malondialdehyde level) and decreased antioxidant status (superoxide dismutase and catalase activities) were found in the co-exposure groups compared with the individual-exposure groups. Meanwhile, severe DNA damage was observed in co-exposure groups. Additionally, the levels of apoptotic (Bax, Caspase-3, Caspase-8, Caspase-9, p53, and PARP) and inflammation (NFκB, Cox-2, TNF-α, and TGFßI) indexes in the co-exposure groups were markedly increased, whereas the levels of anti-apoptosis index (Bcl-2) were decreased. It was also observed that co-exposure with 2,4-D and arsenic caused more histopathological changes in tissues. Generally, these results show that co-exposure to 2,4-D and arsenic can seriously cause oxidative stress, DNA damage, apoptosis and inflammation while having toxicological risk for organisms.
RESUMO
This study showed the protective effect of polydatin (PD), which has an antioxidant activity against oxidative stress in mice caused by aflatoxin B1 (AFB1). In this study, 36 male Swiss albino mice were divided equally into 6 groups: 0.2 mL of FTS was administered to the control group, 0.2 mL of olive oil to the second group, and 0.75 mg/kg AFB1 to the third group by intragastric gavage every day for 28 days. The fourth, fifth, and sixth groups were administered 50, 100, and 200 mg/kg PD and 0.75 mg/kg AFB1 intragastrically for 28 days, respectively. AFB1 administration increased plasma aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, blood urea nitrogen, creatinine, and malondialdehyde levels in blood and tissue samples but decreased the level of glutathione and the activities of superoxide dismutase and catalase. On the other hand, it was determined that PD applications depending on the increasing doses brought these levels closer to normal. In addition, AFB1 administration increased the amount of ssDNA and liver COX-2, TNF-α, IL-6, NFκB, and Cyp3a11 mRNA expression levels; on the other hand, it decreased the IL-2 mRNA expression level. In contrast, increasing doses of PD application regulated the amount of ssDNA and these mRNA expression levels. Additionally, histopathological damage was observed in the liver and kidney tissues of the AFB1 group, while PD applications in a dose-dependent manner improved these damages. As a result, it was determined that PD reduced AFB1-induced oxidative stress, DNA damage, and inflammation and exhibited a protective effect on tissues in mice.