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1.
Chem Biol Interact ; 333: 109333, 2020 Nov 23.
Artículo en Inglés | MEDLINE | ID: mdl-33242462

RESUMEN

Arsenic, a major environmental pollutant of global concern, is well-known for its reproductive toxicity. In this study, the protective potential of chlorogenic acid (CGA), a caffeoylquinic acid isomer abundantly found in many plants, was investigated against sodium arsenite (NaAsO2)-induced testicular dysfunctions. Adult male Swiss mice were either administered NaAsO2 alone at 5 mg kg-1 or co-treated with CGA at 100 mg kg-1 or 200 mg kg-1 body weight for 4 weeks. Results showed that NaAsO2-treated mice exhibited marked declines in testes weight, sperm count, and viability accompanied by decreases in sexual hormonal levels. Moreover, NaAsO2 toxicity evoked exhaustion of antioxidant markers (SOD, CAT, GPx, GR, and GSH), down-regulation of Nrf2 (nuclear factor erythroid 2-related factor 2) gene expression level, and elevations in malondialdehyde. Further, elevations in inflammatory cytokines (IL-1, TNF-α, and IL-6) together with the up-regulation of pro-apoptotic biomarkers (Bax and caspase- 3) and down-regulation of anti-apoptotic Bcl-2 were observed in NaAsO2 intoxication. Immunohistochemical analysis of testis sections of NaAsO2-treated mice showed high caspase-3 expression. These findings were well supported with testicular histopathological examination. However, pretreatment of mice with CGA resulted in noteworthy improvements in testicular damage induced by arsenic in a dose-dependent manner possibly mediated by the Nrf2 signaling pathway. Conclusively, CGA counteracted arsenic-induced testicular injury through its antioxidant, anti-inflammatory, and anti-apoptotic properties. Therefore, CGA could serve as a favorable intervention in the alleviation of arsenic-induced reproductive toxicity.

2.
J Diabetes Res ; 2020: 6762709, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32626781

RESUMEN

Diabetes mellitus (DM) is a chronic endocrine disease characterized by persistent hyperglycemia. Oxidative damage, inflammatory cytokines, and apoptotic cell death play a major role in the induction and progression of male testicular damage. Plant-derived phytochemicals such as green coffee (Coffea arabica) can possess antidiabetic effects with little toxicity. The current study is aimed at investigating the therapeutic roles of green coffee in diabetic testicular injury stimulated by high-fat diet/streptozotocin administration. Diabetes mellitus was induced by a high-fat diet and a single dose of streptozotocin (STZ) (35 mg kg-1) in male albino rats. Diabetic animals were orally given two different concentrations of green coffee (50 mg kg-1 and 100 mg kg-1) for 28 days. The levels of testosterone, luteinizing hormone, and follicle-stimulating hormone and parameters of oxidative stress, inflammation, and apoptosis were measured. mRNAs and protein levels were detected quantitatively by real-time PCR and ELISA, respectively. In the diabetic group, the levels of testosterone, luteinizing hormone, and follicle-stimulating hormone showed a significant reduction while they increased significantly after green coffee treatment. A significant increase of antioxidant markers glutathione, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase along with decreased levels of lipid peroxides and nitric oxide was observed after green coffee treatment in the diabetic group. Finally, the levels of IL-1ß, TNF-α, Bax, and caspase-3 were also decreased in both treated groups (metformin and green coffee) when compared to the diabetic group. We conclude that testicular oxidative impairment induced by a high-fat diet (HFD) and STZ can be reversed by green coffee. Administration of green coffee could represent a promising therapeutic agent which can help the treatment of type 2 DM-induced testicular dysfunction.

3.
J Sci Food Agric ; 100(14): 5162-5170, 2020 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-32519758

RESUMEN

BACKGROUND: Chronic exposure to arsenic (As) leads to serious renal disorders. Chlorogenic acid (CGA), a phenolic compound, has several well known physiological benefits, including antioxidant and anti-inflammatory activities. The present study investigated the potential renoprotective effects of CGA on sodium arsenite (NaAsO2 )-induced kidney damage in mice. The mice were randomly allocated into five groups to receive daily treatment with CGA (200 mg kg-1 ), NaAsO2 (5 mg kg-1 ), NaAsO2 + CGA (100 mg kg-1 ), NaAsO2 + CGA (200 mg kg-1 ), or a control for 28 days. RESULTS: In the NaAsO2 -treated group, NaAsO2 induced significant renal dysfunction, oxidative damage, inflammation, and apoptosis, as demonstrated by marked increases in urea and creatinine levels accompanied by a decrease in the kidney index. Considerable increases in malondialdehyde and nitric oxide levels and parallel decreases in various antioxidant markers (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione) levels were also detected in the renal tissues of NaAsO2 -treated mice. NaAsO2 exposure was associated with marked increases in renal inflammatory markers (interleukin-1ß and tumor necrosis factor-α) and apoptosis indicators including Bax and caspase-3 levels contaminant, with a marked decrease in Bcl-2, an anti-apoptotic protein, in the NaAsO2 -treated group compared with the control group. However, pretreatment with CGA substantially mitigated the renal injury and dysfunction associated with NaAsO2 exposure by reducing tissue inflammation and apoptosis and improving the antioxidant status. The CGA pretreatment also alleviated the NaAsO2 -induced histological alterations in renal tissues. CONCLUSION: Taken together, our results suggest the efficacy of CGA in alleviating As-mediated renal tissue damage. © 2020 Society of Chemical Industry.

4.
Mediators Inflamm ; 2020: 8508906, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32377166

RESUMEN

Diallyl disulfide (DADS) is the major organosulfur constituent in garlic, with a variety of pharmacological activities including antioxidant and anti-inflammatory. Here, we examined the potential antiedematous impact of DADS- versus carrageenan-mediated paw edema in mice. Carrageenan injection potentiated an inflammatory reaction as presented by the elevated serological C-reactive protein (CRP) levels and transcription of tumor necrosis factor-alpha (TNF-α, Tnfα), interleukin-1 beta (IL-1ß, Il1b), interleukin-2 (IL-2, Il2), inducible nitric oxide synthase (iNOS), nitric oxide (NO), cyclooxygenase-2 (COX-2, Ptgs2), prostaglandin E2 (PGE2), monocyte chemoattractant protein-1 (MCP-1, Ccl1), nuclear factor kappa B (NF-κB), and myeloperoxidase (MPO) activity, while interleukin-10 (IL-10) was declined in the injured paw tissue. Additionally, carrageenan elevated lipid peroxidation in terms of malondialdehyde (MDA) and decreased glutathione content (GSH). Remarkably, DADS was found to inhibit the inflammatory signaling, suppressed the developed oxidative damage, and protected the histopathological alterations in the inflamed paw tissue in response to carrageenan injection. Our findings suggest that DADS could be used as an alternative therapy used to alleviate the pathophysiological changes associated with the genesis of paw edema through its potent anti-inflammatory and antioxidant impacts.

5.
Environ Sci Pollut Res Int ; 27(6): 5981-5992, 2020 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-31863371

RESUMEN

Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride (CdCl2)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), CdCl2 (0.6 mg/kg), and SAE + CdCl2, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1ß) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before CdCl2 exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by CdCl2 exposure. SAE can be used as a promising protective agent against CdCl2-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract.


Asunto(s)
Cloruro de Cadmio/toxicidad , Sustancias Peligrosas/toxicidad , Sustancias Protectoras/farmacología , Extracto de Senna/farmacología , Senna (Planta) , Animales , Antioxidantes , Apoptosis , Cadmio , Suplementos Dietéticos , Hígado , Estrés Oxidativo , Ratas , Senósidos , Superóxido Dismutasa
6.
Int J Mol Sci ; 20(22)2019 Nov 11.
Artículo en Inglés | MEDLINE | ID: mdl-31718011

RESUMEN

The present study aimed to test the anti-inflammatory and xanthine oxidase inhibitory activities of two synthesized molecules and compare them to routinely prescribed nonsteroidal anti-inflammatory drugs (NSAIDs), such as diclofenac and the serum urate-lowering drug, allopurinol. The anti-inflammatory effects of the designed compounds (A and B) were evaluated in carrageenan (CAR)-induced paw edema in mice. The levels of nitric oxide and myeloperoxidase activity were measured in paw skin using biochemical methods. Additionally, prostaglandin E2 (PGE2), C-reactive protein (CRP), cyclooxygenase-2 (Cox-2), tumor necrosis factor-α (TNFα), interleukin (IL)-1ß, IL-2 and IL-10, and monocyte chemoattractant protein-1 (MCP1) were assessed by enzyme-linked immunosorbent assay (ELISA). The expression of inflammation-related genes was confirmed by real-time qPCR. The expression of inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-κB) were estimated using immunohistochemistry, and xanthine oxidase inhibitory activity was evaluated using an in vitro assay. The results revealed that compounds A and B decreased inflammation, as was observed by a reduction in the elevation of all the tested markers. In addition, the tested compounds markedly decreased paw swelling, mobilization of inflammatory cells, iNOS-, and NF-κB-immunoreactive cells in a mouse model of paw edema. Interestingly, both compounds were potent xanthine oxidase inhibitors as well as Cox inhibitors with higher activity in favor of compound B providing potential dual acting series of anti-hyperuricemic and anti-inflammatory therapeutic agents.


Asunto(s)
Antiinflamatorios/farmacología , Edema/tratamiento farmacológico , Supresores de la Gota/farmacología , Animales , Antiinflamatorios/química , Antiinflamatorios/uso terapéutico , Proteína C-Reactiva/análisis , Células Cultivadas , Quimiocina CCL2/metabolismo , Ciclooxigenasa 2/metabolismo , Dinoprostona/metabolismo , Supresores de la Gota/química , Supresores de la Gota/uso terapéutico , Interleucinas/metabolismo , Masculino , Ratones , FN-kappa B/metabolismo , Óxido Nítrico/metabolismo , Óxido Nítrico Sintasa de Tipo II/metabolismo , Peroxidasa/metabolismo , Piel/efectos de los fármacos , Piel/metabolismo , Piel/patología , Factor de Necrosis Tumoral alfa/metabolismo , Xantina Oxidasa/antagonistas & inhibidores
7.
Metab Brain Dis ; 34(3): 853-864, 2019 06.
Artículo en Inglés | MEDLINE | ID: mdl-30919246

RESUMEN

Current therapeutic interventions for memory loss are inadequate and are associated with numerous adverse effects. There is an urgent need for new alternative agents for the treatment of memory loss and related disorders. Here, we investigated the potential neuroprotective role of soursop fruit extract (SSFE) in scopolamine (SCO)-induced amnesia and oxidative damage in the hippocampus of rats. Thirty-five rats were randomly allocated into 5 groups: control, SCO, SSFE, SCO, SSFE+SCO and N-acetylcysteine (NAC) + SCO. SCO-treatment increased acetylcholine esterase activity and decreased hippocampal levels of acetylcholine, serotonin, dopamine, norepinephrine, and histamine. The level of ATP increased. SCO-treated rats showed a disturbance in oxidative status, which was evident through the increase in malondialdehyde, and nitrites/nitrates and a decrease in cellular antioxidant molecules including glutathione, superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase. A disturbance was also observed via downregulation of the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 defense pathways. SCO-treatment enhances a neuroinflammatory state, as indicated by the release of tumor necrosis factor- α and interleukin-1ß and increased inducible nitric oxide synthase and mRNA expression. SCO-treatment decreased the expression of the anti-apoptotic protein, B cell lymphoma 2 and increased the expression of the pro-apoptotic protein, Bcl-2 associated X protein, caspase-3 and cytochrome c in hippocampal neurons. SSFE pretreatment markedly ameliorated hippocampal changes. Our findings revealed that SSFE exerts its potential anti-amnestic effect mainly through the activation of the cholinergic system and Nrf2/HO-1 pathway.


Asunto(s)
Acetilcolina/farmacología , Hemo-Oxigenasa 1/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Escopolamina/farmacología , Amnesia/inducido químicamente , Amnesia/tratamiento farmacológico , Animales , Antioxidantes/farmacología , Hemo-Oxigenasa 1/genética , Masculino , Malondialdehído/metabolismo , Malondialdehído/farmacología , Óxido Nítrico Sintasa de Tipo II/efectos de los fármacos , Óxido Nítrico Sintasa de Tipo II/metabolismo , Ratas Wistar
8.
Biosci Rep ; 38(6)2018 12 21.
Artículo en Inglés | MEDLINE | ID: mdl-30291211

RESUMEN

Cadmium (Cd) is a common environmental toxicant that has harmful effects on plants, animals, and humans. The present study evaluated the protective effects of Fragaria ananassa methanolic extract (SME) on cadmium chloride (CdCl2)-induced neuronal toxicity in rats. Male albino rats were intraperitoneally (i.p) injected with CdCl2 (6.5 mg/kg) for 5 days with or without the SME (250 mg/kg). We measured the levels of Cd, lipid peroxidation (LPO), nitric oxide, glutathione (GSH), and oxidative enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase, and glutathione reductase (GR) in the whole brain homogenate. Compared with the control group, the Cd-intoxicated group showed a marked increase in the brain levels of Cd, LPO, and nitric oxide and a decrease in the levels of GSH and all tested antioxidant enzymes. Compared with Cd-intoxicated rats, the rats pretreated with SME showed restoration of oxidative balance in the brain tissue. While the expression of brain SOD2, CAT, glutathione peroxidase 1, and GR was down-regulated in the Cd-treated group, the expression of these enzymes was up-regulated in rats pretreated with SME. In addition, administration of SME before CdCl2 increased the Bcl-2 expression, but significantly decreased the expression of Bax. Immunohistochemical analysis showed that compared with Cd-intoxicated rats, rats pretreated with SME showed a decrease in the protein expression of tumor necrosis factor α (TNF-α). Our findings indicate that SME protects the brain tissue from Cd-induced neuronal toxicity by improving the antioxidant system and increasing antiapoptotic and anti-inflammatory activities.


Asunto(s)
Cloruro de Cadmio/toxicidad , Fragaria/química , Neuronas/efectos de los fármacos , Extractos Vegetales/administración & dosificación , Animales , Antioxidantes/administración & dosificación , Antioxidantes/química , Apoptosis/efectos de los fármacos , Regulación de la Expresión Génica/efectos de los fármacos , Humanos , Peroxidación de Lípido/efectos de los fármacos , Neuronas/patología , Oxidación-Reducción/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Extractos Vegetales/química , Sustancias Protectoras/administración & dosificación , Sustancias Protectoras/química , Ratas , Factor de Necrosis Tumoral alfa/genética
9.
J Enzyme Inhib Med Chem ; 33(1): 755-767, 2018 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-29651867

RESUMEN

In this research, we exploited derivatives of thieno[2,3-b]pyridine as dual inhibitors of the key enzymes in eicosanoid biosynthesis, cyclooxygenase (COX, subtypes 1 and 2) and 5-lipoxygensase (5-LOX). Testing these compounds in a rat paw oedema model revealed potency higher than ibuprofen. The most active compounds 7a, 7b, 8b, and 8c were screened against COX-1/2 and 5-LOX enzymes. Compound 7a was the most powerful inhibitor of 5-LOX with IC50 = 0.15 µM, while its p-chloro analogue 7b was more active against COX-2 (IC50 = 7.5 µM). The less desirable target COX-1 was inhibited more potently by 8c with IC50 = 7.7 µM. Surflex docking programme predicted that the more stable anti- conformer of compound (7a) formed a favourable complex with the active site of 5-LOX but not COX-1. This is in contrast to the binding mode of 8c, which resembles the syn-conformer of series 7 and binds favourably to COX-1.


Asunto(s)
Antiinflamatorios no Esteroideos/farmacología , Inhibidores de la Ciclooxigenasa/farmacología , Edema/tratamiento farmacológico , Eicosanoides/antagonistas & inhibidores , Inhibidores de la Lipooxigenasa/farmacología , Piridinas/farmacología , Animales , Antiinflamatorios no Esteroideos/síntesis química , Antiinflamatorios no Esteroideos/química , Araquidonato 5-Lipooxigenasa/metabolismo , Inhibidores de la Ciclooxigenasa/síntesis química , Inhibidores de la Ciclooxigenasa/química , Relación Dosis-Respuesta a Droga , Eicosanoides/biosíntesis , Eicosanoides/química , Inhibidores de la Lipooxigenasa/síntesis química , Inhibidores de la Lipooxigenasa/química , Masculino , Modelos Moleculares , Estructura Molecular , Prostaglandina-Endoperóxido Sintasas/metabolismo , Piridinas/síntesis química , Piridinas/química , Ratas , Ratas Sprague-Dawley , Relación Estructura-Actividad
10.
Food Chem Toxicol ; 115: 49-62, 2018 May.
Artículo en Inglés | MEDLINE | ID: mdl-29518435

RESUMEN

In this study, we aimed to evaluate the anti-inflammatory and protective effects of Ziziphus spina-christi fruit extract (ZFE) against acetic acid (AcOH)-induced colitis in rats. Before a single AcOH instillation, ZFE (100, 200, and 400 mg/kg/day) was administered for 5 days by oral gavage. Pretreatment with ZFE at different doses suppressed the spread of inflammation and inhibited mucosal damage; in addition, it reduced ulcer size and mitigated colitis markers. Administration of ZFE (400 mg/kg) resulted in a greater reduction of inflammatory colonic injury than that after reference drug, mesalazine (MLZ), administration. In addition, ZFE not only histopathologically ameliorated AcOH-induced colitis but also restored the balance between the oxidants and antioxidants. Furthermore, ZFE effectively modulated the mRNA expression of redox-sensitive transcription factors, such as nuclear factor (erythroid-derived 2)-like 2 and heme oxygenase-1, downregulated the expression of p38 mitogen-activated protein kinase, and upregulated that of vascular endothelial growth factor A and interleukin-1ß in AcOH-induced colitis in rats. In conclusion, our results suggested that ZFE could prevent the development of chronic experimental colitis in rats; therefore, it could be considered as an alternative and/or additive therapeutic approach for the management of inflammatory bowel disease.


Asunto(s)
Colitis Ulcerosa/tratamiento farmacológico , Colitis Ulcerosa/metabolismo , Hemo-Oxigenasa 1/genética , Factor 2 Relacionado con NF-E2/genética , Estrés Oxidativo/efectos de los fármacos , Extractos Vegetales/administración & dosificación , Ziziphus/química , Proteínas Quinasas p38 Activadas por Mitógenos/genética , Animales , Colitis Ulcerosa/genética , Frutas/química , Hemo-Oxigenasa 1/metabolismo , Humanos , Masculino , Factor 2 Relacionado con NF-E2/metabolismo , Ratas , Ratas Wistar , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo
11.
Ren Fail ; 38(8): 1267-75, 2016 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-27435113

RESUMEN

Glomerular filtration rate and/or creatinine are not accurate methods for renal failure prediction. This study tested homocysteine (Hcy) as a predictive and prognostic marker for end stage renal disease (ESRD). In total, 176 subjects were recruited and divided into: healthy normal group (108 subjects); mild-to-moderate impaired renal function group (21 patients); severe impaired renal function group (7 patients); and chronic renal failure group (40 patients) who were on regular hemodialysis. Blood samples were collected, and serum was separated for analysis of total Hcy, creatinine, high sensitive C-reactive protein (CRP), serum albumin, and calcium. Data showed that Hcy level was significantly increased from normal-to-mild impairment then significantly decreases from mild impairment until the patient reaches severe impairment while showing significant elevation in the last stage of chronic renal disease. Creatinine level was increased in all stages of kidney impairment in comparison with control. CRP level was showing significant elevation in the last stage. A significant decrease in both albumin and calcium was occurred in all stages of renal impairment. We conclude Hcy in combination with CRP, creatinine, albumin, and calcium can be used as a prognostic marker for ESRD and an early diagnostic marker for the risk of renal failure.


Asunto(s)
Proteína C-Reactiva/análisis , Creatinina/sangre , Progresión de la Enfermedad , Diagnóstico Precoz , Homocisteína/sangre , Fallo Renal Crónico/sangre , Adulto , Biomarcadores/sangre , Calcio/sangre , Estudios de Casos y Controles , Egipto , Femenino , Tasa de Filtración Glomerular , Humanos , Fallo Renal Crónico/diagnóstico , Fallo Renal Crónico/terapia , Masculino , Persona de Mediana Edad , Análisis Multivariante , Diálisis Renal , Albúmina Sérica
12.
Neuropsychiatr Dis Treat ; 11: 1067-76, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-25926735

RESUMEN

BACKGROUND: The current study's aim is to evaluate the possible interaction effects of khat chewing on treatment of paranoid schizophrenic patients. PATIENTS AND METHODS: In the study group, 42 male subjects suffered from paranoid schizophrenia and were classified according to their khat chewing habits into two subgroups: either khat-chewer subgroup (SKc; n=21; r=11, h=10) or non-khat-chewer subgroup (SNKc; n=21, r=11, h=10). Each subgroup was further subdivided according to type of treatment into r (risperidone) and h (haloperidol). Healthy male subjects (37) were subdivided into healthy khat-chewer as positive controls (HKc, n=17) and healthy non-khat-chewer as negative controls (HNKc, n=20). Plasma dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid, 5-hydroxytryptamine (serotonin), 5-hydroxyindoleacetic acid, epinephrine, and norepinephrine were estimated. RESULTS: ANOVA and post hoc analysis showed that dopamine was illustrating significant elevation in all khat chewing groups. DOPAC was illustrating significant decrease in all khat chewing groups with an interesting outcome showing significant increase in DOPAC in SNKcr group due to risperidone effect. Homovanillic acid, serotonin, hydroxyindoleacetic acid, and norepinephrine were illustrating significant elevations in all khat chewing groups. Epinephrine was illustrating significant elevation in all chewers than non-chewers groups. Unexpected significant decrease in epinephrine in the SNKcr group indicated that risperidone drug is decreasing epinephrine through indirect mechanism involving calcium. CONCLUSION: Khat chewing in schizophrenic patients is contraindicated because it aggravates the disease symptoms, attenuates all used treatment medications, and deteriorates all biochemical markers of the patients.

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