Erika Daniela González-Renovato

Role of the Blood–Brain Barrier in Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system associated with demyelination and axonal loss eventually leading to neurodegeneration. MS exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the blood-brain barrier (BBB). The BBB is a complex organization of cerebral endothelial cells, pericytes and their basal lamina, which are surrounded and supported by astrocytes and perivascular macrophages. In pathological conditions, lymphocytes activated in the periphery infiltrate the central nervous system to trigger a local immune response that ultimately damages myelin and axons. Cytotoxic factors including pro-inflammatory cytokines, proteases, and reactive oxygen and nitrogen species accumulate and may contribute to myelin destruction. Dysregulation of the BBB and transendothelial migration of activated leukocytes are among the earliest cerebrovascular abnormalities seen in MS brains and parallel the release of inflammatory cytokines. In this review we establish the importance of the role of the BBB in MS. Improvements in our understanding of molecular mechanism of BBB functioning in physiological and pathological conditions could lead to improvement in the quality of life of MS patients.

NutriSim© Protects-Against Apoptosis in Hippocampus Induced by Transient Ischemia in Mongolian Gerbils (Meriones Unguiculatus)

Mongolian gerbil model has been extensively used for the study of neuroprotective drugs since transient bilateral common carotid artery occlusion induces neuronal cell death to selectively vulnerable regions, including the CA1 sector of the hippocampus. Previously we have shown that NutriSim©, a nutritive supplement used empirically in the treatment of several degenerative disorders protects against brain damage induced by ischemia-reperfusion in Mongolian gerbils. These effects are partly attributed to its antioxidant action. The purpose of this study was to further investigate the potential neuroprotective effects of NutriSim© with histological measures of global ischemia in gerbils. We found that a single dose of NutriSim© was able to prevent significantly the ischemia-induced pyramidal cell loss as well as the number of hyperchromatic cells and glial cells after a week of treatment. In consonance with these data, increased TUNEL positive cells after ischemia is reduced in NutriSim© treated animal after a week.

Spinal muscular atrophy: review of a child onset disease.

Laboratorio de Desarrollo-Envejecimiento, Enfermedades Neurodegenerativas, Centro de Investigacion Biomedica de Occidente, Instituto Mexicano del Seguro Social. Sierra Mojada 800, 44243, Guadalajara, Jalisco, Mexico. 2 Centro Universitario de Ciencias de la Salud (CUCS), University of Guadalajara, Guadalajara, Jalisco, Mexico. Asociacion Mexicana de Atrofia Muscular Espinal (AMAME), Guadalajara Jalisco, Mexico. 4 Department of Internal Medicine, University of Iowa Hospital and Clinics, Iowa, USA. Centro Universitario de Ciencias Exactas e Ingenierias, University of Guadalajara, Guadalajara, Jalisco, Mexico.

Multiple Sclerosis and Its Relationship with Oxidative Stress, Glutathione Redox System, ATPase System, and Membrane Fluidity

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) with a focus on inflammation, demyelination, and damage to axons leading to neurological deficits. MS pathology is associated with excessive reactive oxygen species (ROS) and generation of reactive nitrogen species (RNS), causing oxidative/nitrosa‐ tive stress. Deregulation of glutathione homeostasis and alterations in glutathione‐ dependent enzymes are implicated in MS. Reactive oxygen species enhance both monocyte adhesion and migration across brain endothelial cells. In addition, ROS can activate the expression of the nuclear transcription factor‐kappa, which upregulates the expression of many genes involved in MS, such as tumor necrosis factor‐α and nitric oxide synthase, among others, leading to mitochondrial dysfunction and energy deficits that result in mitochondrial and cellular calcium overload. Loss of mitochondrial membrane potential can increase the release of cytochrome c, one pathway that leads to neuronal apoptosis. Clinical studies suggest that omega‐3 long‐chain polyunsaturat‐ ed fatty acids (PUFAs) including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have anti‐inflammatory, antioxidant, and neuroprotective effects in MS and animal models of MS. Here, we review the relationship of oxidative stress, the

Oxidative Stress and Parkinson’s Disease: Effects on Environmental Toxicology

Epidemiological studies have found an increased risk of Parkinson’s disease (PD) with environmental factors such as exposure to substances derived from industrial processes, use of agrochemicals, or living in a rural environment. The hypothesis that certain environmental toxins could be the source of the EP is supported by the discovery that chemicals such as herbicides paraquat, diquat, and the fungicide maneb are selectively toxic in nigrostriatal dopaminergic neurons. Also, one of the insecticides produced by plants, such as rotenone, and by-product of the synthesis of synthetic heroin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) can be reproduced in animal models where neurochemicals, histopathological, and clinical characteristic of PD can be found. Interestingly, there are similarities in the chemical structure of paraquat and MPTP. Recent evidence exhibited that inflammation and oxidative stress play an essential role in the development of PD. So, in our laboratory we found that in an animal model melatonin decreases the products of lipid oxidation, nitric oxide metabolites, and the activity of cyclooxygenase 2, which are induced by an intraperitoneal injection of MPTP. This suggests that the neuroprotective effects of melatonin are partially attributed to its antioxidant scavenging and anti-inflammatory action.

Efficacy of Symbiotics in an Experimental Model of Endotoxic Shock Induced by Lipopolysaccharide from Escherichia Coli

Obsevation: Endotoxic shock is a life-threatening condition and its sequelae represent an array of clinical symptoms that encompass systemic inflammation, coagulopathy, and abnormalities of the renal, hepatic, pulmonary and hematologic systems, followed by multi-organ failure. Furthermore, systemic failure leads to an unfavorable environment in the gut that causes an imbalance in the homeostasis of intestinal microbiota. In the present study, the effect of symbiotics as adjuvant therapy in endotoxic shock was investigated. Adult male Wistar rats were randomized into three groups: Control group received a single intraperitoneal injection of physiological saline solution, and the other two groups received either a symbiotic formulation or a placebo daily, for one week, followed by the administration of a single lethal dose of lipopolysaccharide (LPS) from E. coli (20 mg/Kg, IP). Results: The symbiotic formulation used improved the survival rate of LPS-treated rats, ameliorated the clinical symptomatology, reduced the production of serum proinflammatory cytokines (TNF-α, IL-6, IL-1β), and preserved the mitochondrial membrane fluidity and ATPase activity. Conclusion: The symbiotic formulation used as a pre-treatment in this experimental model, reduced mortality and showed beneficial effects at the systemic and sub-cellular levels. *Corresponding author: Dr. Genaro Gabriel Ortiz, DevelopmentAging Laboratory, Neurodegenerative diseases, Division of Neurosciences, CIBO-IMSS, Sierra Mojada 800 CP 44340. Guadalajara, Jalisco, Mexico, Tel: (0133) 2015 3651; E-mail: genarogabriel@yahoo.com Received Date: April 13, 2016 Accepted Date: June 06, 2016 Published Date: June 09, 2016

Cross-talk between glial cells and neurons: Relationship in Multiple Sclerosis.

Laboratorio Desarrollo-Envejecimiento; Enfermedades Neurodegenerativas. Division de Neurociencias. Centro de Investigacion Biomedica de Occidente (CIBO). Instituto Mexicano del Seguro Social (IMSS), Guadalajara, Jal. Mexico Departamento de Biologia molecular y genomica. Centro Universitario de Ciencias de la Salud (CUCS). Universidad de Guadalajara. Guadalajara, Jal. Mexico Departamento de Quimica. Centro Universitario de Ciencias Exactas e Ingenierias. Universidad de Guadalajara. Guadalajara, Jal. Mexico Departamento de Neurologia. Unidad Medica de Alta Especialidad (UMAE). Hospital de Especialidades (HE). Centro Medico Nacional de Occidente (CMNO), IMSS, Guadalajara, Jal. Mexico. Departamento de Investigacion, Centro Universitario de Los Altos, Universidad de Guadalajara.

Effect of combined aerobic and anaerobic training on hemodynamic response, serum oxidative stress markers and platelet ATP synthase activities in patients with coronary heart disease: a pilot study.

1 Axial. Medicina de Rehabilitacion y Desarrollo Infantil CS. Guadalajara, Jalisco, Mexico. Laboratorio de Mitocondria-Estres Oxidativo & Enfermedad, Centro de Investigacion Biomedica de Occidente (CIBO), Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, Mexico. 3 Departamento de Quimica, Centro Universitario de Ciencias Exactas e Ingenierias, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico. 4 Departamento de Readaptacion Cardiovascular, Instituto Cardiovascular de Guadalajara (ICG), Hospital Bernardette, Guadalajara, Jalisco, Mexico.