Antioxidant properties of natural compounds used in popular medicine for gastric ulcers

There is evidence concerning the participation of reactive oxygen species in the etiology and physiopathology of human diseases, such as neurodegenerative disorders, inflammation, viral infections, autoimmune pathologies, and digestive system disorders such as gastrointestinal inflammation and gastric ulcer. The role of these reactive oxygen species in several diseases and the potential antioxidant protective effect of natural compounds on affected tissues are topics of high current interest. To consider a natural compound or a drug as an antioxidant substance it is necessary to investigate its antioxidant properties in vitro and then to evaluate its antioxidant functions in biological systems. In this review article, we shall consider the role of natural antioxidants derived from popular plants to reduce or prevent the oxidative stress in gastric ulcer induced by ethanol

Alzheimer disease and cognitive impairment associated with diabetes mellitus type 2: associations and a hypothesis

Introduction: Epidemiological studies have demonstrated that patients with diabetes mellitus have an increased risk of developing Alzheimer disease, but the relationship between the 2 entities is not clear. Development: Both diseases exhibit similar metabolic abnormalities: disordered glucose metabolism, abnormal insulin receptor signalling and insulin resistance, oxidative stress, and structural abnormalities in proteins and β-amyloid deposits. Different hypotheses have emerged from experimental work in the last two decades. One of the most comprehensive relates the microvascular damage in diabetic polyneuritis with the central nervous system changes occurring in Alzheimer disease. Another hypothesis considers that cognitive impairment in both diabetes and Alzheimer disease is linked to a state of systemic oxidative stress. Recently, attenuation of cognitive impairment and normalisation of values in biochemical markers for oxidative stress were found in patients with Alzheimer disease and concomitant diabetes. Antidiabetic drugs may have a beneficial effect on glycolysis and its end products, and on other metabolic alterations. Conclusions: Diabetic patients are at increased risk for developing Alzheimer disease, but paradoxically, their biochemical alterations and cognitive impairment are less pronounced than in groups of dementia patients without diabetes. A deeper understanding of interactions between the pathogenic processes of both entities may lead to new therapeutic strategies that would slow or halt the progression of impairment. Resumen: Introducción: Varios estudios epidemiológicos han demostrado que los pacientes de diabetes mellitus de tipo 2 presentan un aumento de riesgo para adquirir enfermedad de Alzheimer, pero las relaciones entre ellas no están aclaradas. Desarrollo: Ambas enfermedades presentan similares anormalidades metabólicas: Alteraciones en el metabolismo de la glucosa, irregularidades en los receptores para la señalización de la insulina, estrés oxidativo, anomalías en la conformación de proteínas y depósitos de β-amiloide. A través del desarrollo de investigaciones experimentales en las últimas 2 décadas, han sido postuladas diversas hipótesis. Una de las más llamativas relaciona los daños microvasculares de la polineuritis diabética con los cambios que se producen en el sistema nervioso central en la enfermedad de Alzheimer. Otra hipótesis considera que en ambas enfermedades la evolución del deterioro cognitivo está vinculada con el estado de estrés oxidativo sistémico. Más recientemente, en pacientes con enfermedad de Alzheimer con diabetes mellitus de tipo 2 concomitante, se ha comprobado la existencia de atenuación en el deterioro cognitivo y la normalización en los valores de variables bioquímicas marcadoras del estrés oxidativo. Los fármacos antidiabéticos podrían ejercer un efecto favorable sobre la glucólisis, sus productos finales y otras alteraciones metabólicas. Conclusiones: Los pacientes diabéticos presentan mayor riesgo para desarrollar Alzheimer, pero, paradójicamente, las alteraciones bioquímicas y el deterioro cognitivo resultan menores que en los grupos de pacientes dementes sin diabetes mellitus. La mejor comprensión de las patogenias que interactúan en estas enfermedades quizás sustente nuevas estrategias terapéuticas conducentes a disminuir o detener la progresión de los deterioros. Keywords: Diabetes mellitus type 2, Alzheimer disease, Cerebral glucose metabolism, Insulin resistance, Oxidative stress, Hypoglycaemic drugs, Palabras clave: Diabetes mellitus de tipo 2, Enfermedad de Alzheimer, Metabolismo cerebral de la glucosa, Resistencia a la insulina, Estrés oxidativo, Fármacos hipoglucémico

KSHV sequences in biopsies and cultured spindle cells of epidemic, iatrogenic and Mediterranean forms of Kaposi's sarcoma.

The pathogenesis of Kaposi's sarcoma (KS) is still unclear, and several factors appear to be involved in the onset of the Kaposi's lesion. Epidemiological studies suggest that a common infective agent may contribute to KS. Sequences which appear to represent a new gammaherpesvirus, currently termed KSHV/HHV8, have recently been identified in KS. To further examine the relationship between this virus and KS, we obtained biopsy samples of KS lesions; these samples, the spindle cells cultured from these lesions and the PBMC of the same patients were tested for the presence of KSHV sequences by PCR. In addition, we tested several ''late passage'' KS spindle cell lines as well as control samples. The biopsy samples were from lesions of the following forms of KS: one sporadic KS, two epidemic KS and three iatrogenic KS, one of which was in the process of regressing after reduction of immunosuppressive therapy, and two that were at different stages (patch and nodular) from a single patient. The sporadic KS specimen was positive, as were the PBMCs from this patient, and cells grown from this biopsy appeared to contain KSHV viral sequences up to the fifth passage. Both epidemic KS biopsies were positive, but in these cases KSHV sequences were not detected in the cultured cells. The biopsy from the regressing iatrogenic KS lesion was negative, as were the cells cultured from this lesion. However, the PBMCs of this patient were weakly positive for KSHV at the time of biopsy, and PBMCs collected from this patient one month later were completely negative. The samples of both the patch and the nodular KS lesions obtained from another immunosuppressed patient showed amplifiable sequences of KSHV, but both the PBMCs of this patient and primary KS cell cultures from these biopsies were negative. Of the late-passage KS lines tested, only one, IST AIDS KS 12, was positive for KSHV. This line is derived from an early angiomatous-macula lesion. Taken together, these data suggest that an active KSHV infection is associated with KS and that elimination of KSHV from the lesion precedes regression of the lesion, strongly correlating KSHV with KS. In addition, early KS lesions may have a higher KSHV burden, or contain cells more susceptible to KSHV infection, further linking KSHV to KS