Efeito protetor do pré-tratamento com ácido ascóbico em modelo experimental de isquemia-reperfusão intestinal: um estudo histomorfométrico

BACKGROUND: Ascorbic acid has shown promise in attenuation of intestinal ischemia-reperfusion (I/R) injury. The aim of this study was to determine the protective effects of ascorbic acid on intestinal morphology during IR injury in rats. MATERIALS AND METHODS: We examined morphological changes in the small intestine of Wistar rats after (i) 40 minutes of ischemia (I), (ii) ischemia followed by 30 min of reperfusion (IR), (iii) ischemia with ascorbic acid (IA), (iv) ischemia followed by reperfusion and ascorbic acid (IRA) and (v) in a sham group (S). We used morphometry to evaluate the amount of villous architecture, crypts, necrosis, hemorrhagic infarcts and inflammatory cells at the mesenteric and antimesenteric borders of the small intestine. RESULTS: Ascorbic acid caused a significant reduction of antimesenteric villous hemorrhagic infarction (pINTRODUÇÃO: O ácido ascórbico tem se mostrado como um agente promissor na atenuação da lesão causada pela isquemia/reperfusão (IR). O objetivo deste estudo foi determinar os efeitos protetores do ácido ascórbico na morfologia intestinal durante a IR em ratos. MATERIAL E MÉTODOS: Examinamos alterações morfológicas no intestino delgado de ratos do tipo Wistar. Após 40 minutos de isquemia (I), isquemia seguida de reperfusão (IR), isquemia com tratamento com ácido ascórbico (IA), isquemia seguida por 30 minutos de reperfusão e tratamento com ácido ascórbico (IRA) e do grupo sham (S). Utilizamos a morfometria para avaliar quantitativamente a arquitetura dos vilos da mucosa intestinal, criptas intestinais, necrose, hemorragia, células inflamatórias nas bordas mesentéricas e antimesentéricas do intestino delgado. RESULTADOS: O ácido ascórbico causou uma redução significativa (

Kefir administration reduced progression of renal injury in STZ-diabetic rats by lowering oxidative stress

This study aimed at assessing the effects of Kefir, a probiotic fermented milk, on oxidative stress in diabetic animals. the induction of diabetes was achieved in adult male Wistar rats using streptozotocin (STZ). the animals were distributed into four groups as follows: control (CTL); control Kefir (CTLK); diabetic (DM) and diabetic Kefir (DMK). Starting on the 5th day of diabetes, Kefir was administered by daily gavage at a dose of 1.8 mL/day for 8 weeks. Before and after Kefir treatment, the rats were placed in individual metabolic cages to obtain blood and urine samples to evaluate urea, creatinine, proteinuria, nitric oxide (NO), thiobarbituric acid reactive substances (TBARS) and C-reactive protein (CRP). After sacrificing the animals, the renal cortex was removed for histology, oxidative stress and NOS evaluation. When compared to CTL rats, DM rats showed increased levels of glycemia, plasmatic urea, proteinuria, renal NO, superoxide anion, TBARS, and plasmatic CRP; also demonstrated a reduction in urinary urea, creatinine, and NO. However, DMK rats showed a significant improvement in most of these parameters. Despite the lack of differences observed in the expression of endothelial NO synthase (eNOS), the expression of inducible NO synthase (iNOS) was significantly lower in the DMK group when compared to DM rats, as assessed by Western blot analysis. Moreover, the DMK group presented a significant reduction of glycogen accumulation within the renal tubules when compared to the DM group. These results indicate that Kefir treatment may contribute to better control of glycemia and oxidative stress, which is associated with the amelioration of renal function, suggesting its use as a non-pharmacological adjuvant to delay the progression of diabetic complications. (C) 2014 Elsevier Inc. All rights reserved.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundacao de Apoio a Universidade Federal de São Paulo (FAP-Unifesp)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Universidade Federal de São Paulo, Dept Med, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Pathol, BR-04023900 São Paulo, BrazilUniv São Paulo, Coll Publ Hlth, Dept Nutr, São Paulo, BrazilUniv São Paulo, Dept Biochem & Pharmaceut Technol, São Paulo, BrazilUniv São Paulo, Dept Nephrol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Med, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Pathol, BR-04023900 São Paulo, BrazilWeb of Scienc

Enteroparasites in Riverside Settlements in the Pantanal Wetlands Ecosystem

Background. Intestinal parasites are a major source of health problems in developing countries, where socioeconomic, cultural, and environmental conditions contribute in maintaining the biological cycles of various parasites and facilitating their spread. The objective of this study, conducted in Corumbá, Mato Grosso do Sul state, Brazil, was to investigate the occurrence of intestinal parasites in riverside communities in the South Pantanal wetlands and conduct educational interventions focused on health and environmental preservation. Method. In total, 196 stool samples were tested for parasites using the merthiolate-iodine-formaldehyde concentration (MIFC) technique and spontaneous sedimentation and educational activities were carried out. Results. Enteroparasite prevalence was 72% (65.6–78.2%; 95% CI). Of the 141 positive cases, monoparasitism was found in 34.7%, biparasitism in 23%, and polyparasitism in 14.3%. Entamoeba coli was the most frequent protozoan (70.2%). Among helminths, hookworms were the most prevalent. Enteroparasitosis prevalence did not differ for sex or place of abode but proved higher in individuals older than 10 years. Conclusion. The high positivity rate for enteroparasites found for the communities stems from lack of sanitation and poor personal and environmental hygiene habits, indicating that effective health policies and educational interventions are needed to reduce the current risk levels

Protective effects of ascorbic acid pretreatment in a rat model of intestinal ischemia-reperfusion injury: a histomorphometric study Efeito protetor do pré-tratamento com ácido ascóbico em modelo experimental de isquemia-reperfusão intestinal: um estudo histomorfométrico

BACKGROUND: Ascorbic acid has shown promise in attenuation of intestinal ischemia-reperfusion (I/R) injury. The aim of this study was to determine the protective effects of ascorbic acid on intestinal morphology during IR injury in rats. MATERIALS AND METHODS: We examined morphological changes in the small intestine of Wistar rats after (i) 40 minutes of ischemia (I), (ii) ischemia followed by 30 min of reperfusion (IR), (iii) ischemia with ascorbic acid (IA), (iv) ischemia followed by reperfusion and ascorbic acid (IRA) and (v) in a sham group (S). We used morphometry to evaluate the amount of villous architecture, crypts, necrosis, hemorrhagic infarcts and inflammatory cells at the mesenteric and antimesenteric borders of the small intestine. RESULTS: Ascorbic acid caused a significant reduction of antimesenteric villous hemorrhagic infarction (p<0.05) of the small intestine after ischemia followed by reperfusion as well as villous necrosis reduction at both borders after ischemia (p<0.05). The lesions found in the small intestine were more prominent along the antimesenteric margin. CONCLUSIONS: Ascorbic acid pretreatment has a protective effect against the intestinal morphological lesions induced by ischemia-reperfusion injury in rats.<br>INTRODUÇÃO: O ácido ascórbico tem se mostrado como um agente promissor na atenuação da lesão causada pela isquemia/reperfusão (IR). O objetivo deste estudo foi determinar os efeitos protetores do ácido ascórbico na morfologia intestinal durante a IR em ratos. MATERIAL E MÉTODOS: Examinamos alterações morfológicas no intestino delgado de ratos do tipo Wistar. Após 40 minutos de isquemia (I), isquemia seguida de reperfusão (IR), isquemia com tratamento com ácido ascórbico (IA), isquemia seguida por 30 minutos de reperfusão e tratamento com ácido ascórbico (IRA) e do grupo sham (S). Utilizamos a morfometria para avaliar quantitativamente a arquitetura dos vilos da mucosa intestinal, criptas intestinais, necrose, hemorragia, células inflamatórias nas bordas mesentéricas e antimesentéricas do intestino delgado. RESULTADOS: O ácido ascórbico causou uma redução significativa (p<0,05) no infarto hemorrágico dos vilos intestinais da borda antimesentérica do intestino delgado após isquemia seguida por reperfusão, bem como redução da necrose dos vilos em ambas as bordas após a isquemia (p<0.05). As lesões presentes no intestino delgado foram mais proeminentes na borda antimesentérica. CONCLUSÕES: O pré-tratamento com ácido ascórbico atenuou ou reduziu significativamente as alterações morfológicas no intestino delgado induzidas pela isquemia-reperfusão

Morphological lesions caused by ZIKV infection in the placenta of undernourished mouse dams

Objectives: Zika virus (ZIKV) congenital infection has been linked tosevere birth defects, especially in the CNS. Recent in vivo studiesfound that placental structure is damaged after ZIKV infection, whichmight be responsible for spontaneous abortions and fetal growth restriction.However, it is still unknown how in utero ZIKV infection ismodulated by different environmental factors that could explain theasymmetrical distribution of malformations found along human populationsinfected with ZIKV. As part of a project analyzing the effectsof maternal undernutrition in a murine model of ZIKV infection, theaim of this study was to analyze histological and ultrastructuralchanges induced in the placenta by the combined action of proteinrestriction and ZIKV.Methods: C57BL/6 nulliparous female mice were fed by either a control(Co) diet with 20% protein content or an isocaloric low protein (LP) dietwith 6% of protein. Administration of both diets started 7-10 days beforemating and continued until E15. Infection was performed on E12 byintraperitoneal injection. Resulting experimental groups were: Co/Mock(Control diet, non-infected), Co/ZIKV (Control diet, ZIKV), LP/Mock (Lowprotein diet, non-infected), LP/ZIKV (Low protein/ZIKV). E15 placentaewere fixed in 4% paraformaldehyde for H&E and PAS-staining or inglutaraldehyde for high resolution optic (HRLM) and transmission electronmicroscopy (TEM).Results: While the junctional zone (JZ) of placentae from Co/ZIKV and LP/Mock was slightly altered, the JZ from LP/ZIKV was disorganized, hadmarked cell death and wide maternal blood spaces compared to Co/Mock.The labyrinth of LP/ZIKV was disorganized with poor trophoblastic adhesion,abundant necrosis and vascular alterations as maternal hemorrhage.By TEM analysis, the most important lesions corroborated in LP/ZIKVgroup were the cytoplasmic vacuolization and loss of labyrinthinetrophoblastic chromatin material.Conclusion: The combined effect of maternal undernutrition and ZIKVenhances placental structural damage with potential consequences in thedeveloping offspring.Fil: Barbeito, Claudio Gustavo. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Barbeito Andrés, Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina. Universidad Nacional Arturo Jauretche. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos. Provincia de Buenos Aires. Ministerio de Salud. Hospital Alta Complejidad en Red El Cruce Dr. Néstor Carlos Kirchner Samic. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos; ArgentinaFil: Ferreira, Jéssica. Universidade Federal do Rio de Janeiro; BrasilFil: Cristofolini, Andrea Lorena. Universidad Nacional de Rio Cuarto. Facultad de Agronomia y Veterinaria. Instituto de Ciencias Veterinarias. - Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - Cordoba. Instituto de Ciencias Veterinarias.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Fiorimanti, Mariana Rita. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Río Cuarto. Facultad de Agronomía y Veterinaria. Departamento de Patología Animal. Área de Microscopia Electrónica; ArgentinaFil: Higa, Luiza. Universidade Federal do Rio de Janeiro; BrasilFil: Bellio, María. Universidade Federal do Rio de Janeiro; BrasilFil: Tanuri, Amilcar. Universidade Federal do Rio de Janeiro; BrasilFil: Merkis, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Río Cuarto. Facultad de Agronomía y Veterinaria. Departamento de Patología Animal. Área de Microscopia Electrónica; ArgentinaFil: Cebral, Elisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; ArgentinaFil: Garcez, Patricia. Universidad Nacional de Río Cuarto. Facultad de Agronomía y Veterinaria. Departamento de Patología Animal. Área de Microscopia Electrónica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaInternational Federation of Placenta Associations MeetingCiudad Autónoma de Buenos AiresArgentinaSociedad Latinoamericana de Interacción Materno-Fetal y Placent