Ketorolac and (-)-Epicatechin change retinal GFAP and NRF2 expression on hyperglycemic CD1 mice.

Our objective was to determine whether (-)-Epicatechin administered alone or simultaneously with topical Ketorolac decreased the relative expression of GFAP and modulated the response of Nrf2 in a mouse model with induced hyperglycemia. We found that GFAP and Nrf2 decreased in the groups that received treatments alone or simultaneous during 8 weeks; even when the effect on the Nrf2 was not pronounced, it showed a higher concentration when GFAP decreased. Our results suggest a protective effect of Ketorolac and (-) - Epicatechin, which seem to limit the preclinical retinal damage caused by inflammation in hyperglycemia.

Effect of Eicosapentaenoic Acid on Body Composition and Inflammation Markers in Patients with Head and Neck Squamous Cell Cancer from a Public Hospital in Mexico.

INTRODUCTION: Head and neck cancer patients are at high risk of anorexia-cachexia syndrome and literature shows that Eicosapentaenoic acid (EPA) could regulate it. We aim to determine the EPA effect on body composition and pro-inflammatory markers in patients with head neck cancer. MATERIALS AND METHODS: A randomized single-blind placebo-controlled clinical trial was conducted in patients with head and neck squamous cell cancer who received a polymeric diet with 2 g of EPA or a standard polymeric diet for six weeks before antineoplastic treatment. We assessed body composition by bioelectrical impedance analysis and determined IL-1ß, IL-6, TNF-α and IFN-γ, CRP, serum proteins, and blood count at baseline and at the end of the study. RESULTS: 32 patients received EPA (2 g/day) and 32 became controls. A decrease in serum levels of IL-1ß, IL-6, TNF-α, and IFN-γ was observed in the experimental group, as well as regulation of body weight (-0.3 ± 5.9 vs. -2.1 ± 3.7), lean body mass (-0.2 ± 3.8 vs. -1.3 ± 3.6), body fat mass (0.2 ± 3.5 vs. -1.2 ± 3.8), and quality of life (10 ± 33 vs. 5 ± 34). CONCLUSION: Supplementing with 2 g/day of EPA to head and neck cancer patient during antineoplastic treatment regulates serum pro-inflammatory cytokines, body weight, lean body mass, and improve quality of life.

Effect of caveolin-1 scaffolding peptide and 17beta-estradiol on intracellular Ca2+ kinetics evoked by angiotensin II in human vascular smooth muscle cells.

Caveolae are identifiable plasma membrane invaginations. The main structural proteins of caveolae are the caveolins. There are three caveolins expressed in mammals, designated Cav-1, Cav-2, and Cav-3. It has been postulated that Cav-1 acts as a scaffold protein for signaling proteins; these include ion channels, enzymes, and other ligand receptors like membrane-associated estrogen receptor (ER)alpha or ERbeta. Caveolae-associated membrane proteins are involved in regulating some of the rapid estrogenic effects of 17beta-estradiol. One important system related to the activity of ERalpha and caveolae is the renin-angiotensin system. Angiotensin II (ANG II) has numerous actions in vascular smooth muscle, including modulation of vasomotor tone, cell growth, apoptosis, phosphatidylinositol 3-kinase (PI3K)/Akt activation, and others. Many proteins associated with caveolae are in close relation with the scaffolding domain of Cav-1 (82-101 amino acid residues). It has been proposed that this peptide may acts as a kinase inhibitor. Therefore, to explore the ability of Cav-1 scaffolding peptide (CSP-1) to regulate ANG II function and analyze the relationship between ERalpha and ANG II type 1 and 2 (AT(1) and AT(2)) receptors, we decided to study the effects of CSP-1 on ANG II-induced intracellular Ca(2+) kinetics and the effect of 17beta-estradiol on this modulation using human smooth muscle cells in culture, intracellular Ca(2+) concentration measurements, immuno- and double-immunocytochemistry confocal analysis of receptor expression, immunoblot analysis, and immunocoprecipitation assays to demonstrate coexpression. We hypothesized that CSP-1 inhibits ANG II-mediated increases in intracellular Ca(2+) concentrations by interfering with intracellular signaling including the PI3K/Akt pathway. We also hypothesize that AT(2) receptors associate with Cav-1. Our results show that there is a close association of AT(1), AT(2), and ERalpha with Cav-1 in human arterial smooth muscle cells in culture. CSP-1 inhibits ANG II-induced intracellular signaling.

Efecto del metoprolol sobre la relajación ventricular en el infarto del miocardio experimental / Effect of metaprolol on the ventricular relaxation of experimental myocardial infarction

En las fases iniciales del infarto del miocardio se prolonga el tiempo de la relajación ventricular. Para caracterizar el efecto del metoprolol, un agente ß-bloqueador sobre la constante T, índice derivado de la curva ventricular en la fase de relajación isovolumétrica, se estudiaron 12 perros a los que se les ligó la arteria descendente anterior. La constante T, la presión diastólica ventricular, la frecuencia cardiaca y la presión arterial media, se midieron en forma basal y a los 15, 30, 60, 120, y 180 minutos después de la oclusión. Sirvieron seis perros de control y a otros seis se les administró metoprolol a la dosis de 35 mg/kg/min, durante 5 minutos. Los perros control tuvieron constantes T más prolongadas, mayores niveles de presión diastólica ventricular y mayor hipotensión severa al final del estudio, en comparación con los tratados que mantuvieron la función diastólica y no tuvieron cambios importantes de la presión arterial. El ß-bloqueador disminuye la alteración de la relajación ventricular, preserva la presión de llenado ventricular e impide el desarrollo de hipotensión en este modelo de infarto experimental

La relación entre Chlamydia pneumoniae y las lesiones aterosclerosas aórticas / The relationship between chlamydia pneumoniae and atheosclerotic lesions of the aorta

Aunque los factores aterogénicos más importantes han sido extensamente estudiados, hay otros más cuya verdadera importancia causal no ha sido bien definida. Existen evidencias patológicas e inmunológicas acerca del papel de diversos agentes infecciosos en la génesis o el desarrollo de la aterosclerosis. Recientemente se ha ligado a la Chlamydia pneumoniae con la aterogénesis al encontrarse evidencia inmunológica de la presencia de este germen en lesiones ateromatosas humana. Se estudiaron 16 especímenes de aortas, obtenidos en autopsias de individuos muertos por cardiopatía isquémica. Se determinó la infección de Ch. pneumoniae, mediante una técnica de inmunofluorescencia con anticuerpo monoclonal murino específico. La reacción positiva se encontró en placas fibrolípidas avanzadas, no ulceradas, de dos pacientes (13 por ciento), incidencia comparable a la informada en la literatura mundial. No se conoce cuál es la verdadera relación entre la infección y la aterogénesis y si la primera comienza o agrava el proceso ateroscleroso o es un fenómeno independiente del proceso arterial.