Efecto de rosuvastatina sobre la expresión in vitro de pecam-1 en células endoteliales humanas estimuladas con los de porphyromonas gingivalis

La presencia de bacterias periodonto-patógenas como Pophyromonas gingivalis en lesiones ateroscleróticas y procesos de endotoxemias en pacientes con enfermedad periodontal pueden ser factores que desencadenarían a nivel endotelial una respuesta inflamatoria pro-aterosclerótica. La expresión de moléculas de adhesión tras la activación endotelial como PECAM-1 toma gran importancia en la adhesión y migración de monocitos durante el proceso inflamatorio pro-aterosclerótico. El manejo en la reducción de estos marcadores inflamatorios ha motivado a buscar minuciosamente posibles efectos anti-inflamatorios en medicamentos convencionalmente formulados para prevenir el riesgo de enfermedad vascular siendo actualmente la Rosuvastatina un fármaco con potencial antiinflamatorio, por lo que se evaluó sobre la expresión in vitro de PECAM-1 en células HCAEC, estimuladas con LPS de P. gingivalis 33277 mediante la técnica Cell ELISA Fluorométrica, de igual modo se evaluó el efecto del fármaco sobre la viabilidad celular utilizando la prueba espectrofotométrica de resazurina. Los resultados obtenidos demostraron que Rusuvastatina disminuye la expresión de PECAM-1 en células HCAEC de manera concentración dependiente (p<0.05) y no inducen citotoxicidad sobre las células, a concentraciones de 100 uM- 6,5uM durante un periodo de exposición de 24 horas. Los hallazgos de este estudio sugieren que Rosuvastatina posee un perfil farmacológico promisorio dado que posee efectos moduladores en la adhesión, vislumbrando propiedades anti-inflamatorias y un alto rango de seguridad toxicológica.Departamento Administrativo de Ciencia, Tecnología e Innovación [CO] Colciencias1308-519-28960Inducción de disfunción endotelial in vitro por lipopolisacarido de bacterias periodontopaticas e inhibición de la inflamación por resolvina (rvd1) y estatina (rosuvastatina)n

NanoBubble-Mediated Oxygenation: Elucidating the Underlying Molecular Mechanisms in Hypoxia and Mitochondrial-Related Pathologies

Worldwide, hypoxia-related conditions, including cancer, COVID-19, and neuro-degenerative diseases, often lead to multi-organ failure and significant mortality. Oxygen, crucial for cellular function, becomes scarce as levels drop below 10 mmHg (2), triggering mitochondrial dysregulation and activating hypoxia-induced factors (HiFs). Herein, oxygen nanobubbles (OnB), an emerging versatile oxygen delivery platform, offer a novel approach to address hypoxia-related pathologies. This review explores OnB oxygen delivery strategies and systems, including diffusion, ultrasound, photodynamic, and pH-responsive nanobubbles. It delves into the nanoscale mechanisms of OnB, elucidating their role in mitochondrial metabolism (TFAM, PGC1alpha), hypoxic responses (HiF-1alpha), and their interplay in chronic pathologies including cancer and neurodegenerative disorders, amongst others. By understanding these dynamics and underlying mechanisms, this article aims to contribute to our accruing knowledge of OnB and the developing potential in ameliorating hypoxia- and metabolic stress-related conditions and fostering innovative therapies

Rosuvastatin inhibits IL-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans

Aggregatibacter actinomycetemcomitans (A.a) is a Gram negative periodontopathogen that has been highly associated with endocarditis and atherosclerosis. However, the potential mechanisms by which A.a could be contributing to atherosclerosis remain unclear. The purpose of this study was to determine the effect of purified LPS from A.a (Aa-LPS) on the expression of pro-inflammatory molecules (i.e., adhesion molecules, Toll-like receptors and cytokines/chemokines) associated with the pathogenesis of atherosclerosis in human coronary artery endothelial cells (HCAECs), as well as evaluating the potential of Rosuvastatin (RSV) for inhibiting the A.a-induced endothelial responses. HCAECs were stimulated with purified A. a-LPS and cytokine expression levels determined by qPCR and flow cytometry, and TLR2 and TLR4 expression evaluated by ELISA fluorometric assay. The effect of RSV in Aa-LPS-induced pro-inflammatory responses was also studied using similar experimental approaches. A. a-LPS increased the expression of IL-6, IL-8, and TLR2 in HCAECs. No effects in the expression of adhesion molecules were observed. Aa-induced IL-6 and IL-8 production was inhibited by RSV particularly at higher doses. These results suggest that Aa-LPS plays a role in pro-inflammatory endothelial responses that could be contributing to the atherosclerotic process, and the use of statins (i.e., RSV) could be reducing the likelihood for Aa-induced pro-atherosclerotic endothelial responses.Departamento Administrativo de Ciencia, Tecnología e Innovación [CO] Colciencias1308-519-28960Inducción de disfunción endotelial in vitro por lipopolisacarido de bacterias periodontopaticas e inhibición de la inflamación por resolvina (rvd1) y estatina (rosuvastatina)n

Lipopolysaccharides isolated from Eikenella corrodens but not from Porphyromonas gingivalis W83 induce proatherosclerotic inflammatory responses in human coronary artery endothelial cells

Eikenella corrodens and Porphyromonas gingivalis are oral microorganisms associated with the periodontal disease and have been identified in atherosclerotic lesions. The pro-atherosclerotic potential of a periodontopathic species depends on the ability of the strain to infect the endothelium. Lipopolysaccharide (LPS) from atherosclerosis-associated bacteria causes innate inflammatory responses in the pathogenic processes induced by microorganisms. The purpose of this study was to compare the pro-inflammatory responses of human coronary artery endothelial cells (HCAECs) to LPS isolated from E. corrodens 23834 and P. gingivalis W83.Departamento Administrativo de Ciencia, Tecnología e Innovación [CO] Colciencias1308-519-28960Inducción de disfunción endotelial in vitro por lipopolisacarido de bacterias periodontopaticas e inhibición de la inflamación por resolvina (rvd1) y estatina (rosuvastatina)n

Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b

Background:Rosuvastatin exhibits anti-inflammatory effects and reduces periodontal diseases andatherosclerosis; however, its role in regulating periodontopathogen-induced endothelial proinflammatoryresponses remains unclear. The purpose of this study is to determine whether rosuvastatin can reduce theproinflammatory response induced byAggregatibacter actinomycetemcomitans(Aa) in human coronaryartery endothelial cells (HCAECs).Methods:HCAECs were stimulated with purifiedAaserotype b lipopolysaccharide (LPS) (Aa-LPS),heat-killed (HK) bacteria (Aa-HK), or live bacteria. Expression of Toll-like receptors and cellular adhesionmolecules were evaluated by fluorometric enzyme-linked immunosorbent assay. Endothelial cell activationwas evaluated by quantifying nuclear factor (NF)-kappa B-p65 and cytokine expression levels by quan-titative polymerase chain reaction and flow cytometry. Effect of rosuvastatin in expression of the athero-protective factor Kru ̈ppel-like factor 2 (KLF2) and cytokines were also studied using similar approaches.Results:HCAECs showed increased interleukin (IL)-6, IL-8, intercellular adhesion molecule 1, and plateletendothelial cell adhesion molecule 1 expression when stimulated withAa-LPS orAa-HK. NF-kB-p65 activa-tion was induced by all antigens.Aa-induced IL-6 and IL-8 production was inhibited by rosuvastatin, partic-ularly at higher doses. Interestingly, reduced IL-6 and IL-8 levels were observed in HCAECs stimulated withAain the presence of higher concentrations of rosuvastatin. This anti-inflammatory effect correlated witha significant increase of rosuvastatin-inducedKLF2.Conclusions:These results suggestAa-induced proinflammatory endothelial responses are regulatedby rosuvastatin in a mechanism that appears to involveKLF2activation. Use of rosuvastatin to preventcardiovascular disease may reduce risk of endothelial activation by bacterial antigen

Critical-sized mandibular defect reconstruction using human dental pulp stem cells in a xenograft model-clinical, radiological, and histological evaluation

Purpose: This research evaluated clinical, histological, and radiological osseous regeneration in a critical-sized bilateral cortico-medullary osseous defect in model rabbits from New Zealand after receiving a hydroxyapatite matrix and polylactic polyglycolic acid (HA/PLGA) implanted with human dental pulp stem cells (DPSCs). Methods: Eight New Zealand rabbits with bilateral mandibular critical-sized defects were performed where one side was treated with an HA/PLGA/DPSC matrix and the other side only with an HA/PLGA matrix for 4 weeks. Results: An osseointegration was clinically observed as well as a reduction of 70% of the surgical lumen on one side and a 35% on the other. Histologically, there was neo-bone formation in HA/PLGA/DPSC scaffold and angiogenesis. A bone radiodensity (RD) of 80% was radiologically observed achieving density levels similar to mandibular bone, while the treatment with HA/PLGA matrix achieves RD levels of 40% on its highest peaks. Conclusions: HA/PLGA/DPSC scaffold was an effective in vivo method for mandibular bone regeneration in critical-sized defects induced on rabbit models

Memorias : XX Congreso Institucional de Investigaciones

Este documento, recoge 10 resúmenes de los trabajos presentados como resultado del proyecto en investigación sobre salud oral e investigación en ingeniería, salud y medio ambiente y biología, para el XX congreso institucional de investigaciones de la Universidad del Bosque. Los productos obtenidos como parte de la investigación son: (1) Condición periodontal en pacientes colombianos con artritis idiopática juvenil (AIJ); (2) Efecto del ácido hipocloroso sobre el sistema amortiguador del pH de la saliva. Estudio in vitro e in vivo; (3) Efecto oxidativo del ácido hipocloroso sobre las proteínas salivales: estudio in vitro; (4) Evaluación del ácido hipocloroso como agente antiplaca para uso en la cavidad oral. Parte I: sustantividad, efecto antiplaca y efectos adversos; (5) Identificación de los factores de virulencia de Klebsiella pneumoniae aislada de cavidad oral asociada a fuentes de contaminación exógena; (6) Modulación de la expresión de factores de crecimiento por ácido hipocloroso sobre fibroblastos gingivales humanos; (7) Potencial de diferenciación y expansión neuronal in vitro a partir de Células Troncales de pulpa dental humana; (8) Resolvina D1 inhibe la expresión de moléculas de adhesión en células endoteliales de arteria coronaria humana estimuladas con lipopolisacárido de P. gingivalis. Estudio in vitro; (9) Viabilidad de microorganismos periodontopáticos y bacilos entéricos después del tratamiento con ácido hipocloroso en comparación con clorhexidina; (10) Modelo in vivo de regeneración ósea mandibular a partir de células troncales dentales humanas.Departamento Administrativo de Ciencia, Tecnología e Innovación [CO] Colciencias1308-519-28960Inducción de disfunción endotelial in vitro por lipopolisacarido de bacterias periodontopaticas e inhibición de la inflamación por resolvina (rvd1) y estatina (rosuvastatina)n

El estudiante como sujeto investigador de su realidad : otras voces intercambio de saberes y experiencias de los semilleros de investigación

De acuerdo con la importancia estratégica de la investigación como función sustantiva institucional, el Comité de Investigaciones de la Facultad de Ciencias Económicas, de la Universidad de San Buenaventura Cali, viene adelantando procesos de divulgación y apoyo al quehacer investigativo estudiantil. Para ello realiza el encuentro denominado “Intercambio de saberes y experiencias de los semilleros de investigación en la Facultad de Ciencias Económicas”, en el cual participan diferentes programas de la Universidad e instituciones educativas amigas. El encuentro de estudiantes investigadores de la Facultad de Ciencias Económicas se origina en la necesidad de contar con nuestros propios espacios para dar cuenta del qué, para qué y cómo investigan nuestros jóvenes estudiantes. El evento es una oportunidad para escuchar las distintas voces en el ámbito de las ciencias económicas y afines por el deseo de seguir tras las huellas del tema de interés elegido libremente por nuestros nóveles investigadores.Universidad de San Buenaventura - Cal