RESUMEN
A novel heterometallic metal-porphyrinic framework (MPFs) built from Y and K ions as nods and meso-tetra(4-carboxyphenyl)porphyrin as linkers has been successfully synthesized and characterized. The single crystal X-ray diffraction indicated that this complex 1 exhibited a bilayered architecture of the porphyrins, which is seldom seen in MPFs. In addition, in vitro anticancer activity of complex 1 on three human breast cancer cells (BT474, SKBr-3 and ZR-75-30) was further determined.
Asunto(s)
Humanos , Porfirinas/química , Neoplasias de la Mama/tratamiento farmacológico , Estructuras Metalorgánicas/farmacología , Estructuras Metalorgánicas/química , Antineoplásicos/farmacología , Antineoplásicos/química , Valores de Referencia , Sales de Tetrazolio , Reproducibilidad de los Resultados , Cristalografía por Rayos X , Línea Celular Tumoral , Complejos de Coordinación/farmacología , Complejos de Coordinación/química , FormazánsRESUMEN
The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.
Asunto(s)
Animales , Masculino , Linfa/metabolismo , Oclusión Vascular Mesentérica/complicaciones , Daño por Reperfusión/etiología , Reperfusión/efectos adversos , Bazo/lesiones , Proteínas de Fase Aguda/análisis , Adenosina Trifosfatasas/análisis , /análisis , Proteínas Portadoras/análisis , Endotoxinas/análisis , Molécula 1 de Adhesión Intercelular/análisis , Intestinos/irrigación sanguínea , Arteria Mesentérica Superior , Malondialdehído/análisis , Glicoproteínas de Membrana/análisis , Óxido Nítrico Sintasa/análisis , Óxido Nítrico/análisis , Peroxidasa/análisis , Ratas Wistar , Bazo/patología , Superóxido Dismutasa/análisis , Factor de Necrosis Tumoral alfa/análisisRESUMEN
Notch signaling is an evolutionarily ancient, highly conserved pathway important for deciding cell fate, cellular development, differentiation, proliferation, apoptosis, adhesion, and epithelial-to-mesenchymal transition. Notch signaling is also critical in mammalian cardiogenesis, as mutations in this signaling pathway are linked to human congenital heart disease. Furthermore, Notch signaling can repair myocardial injury by promoting myocardial regeneration, protecting ischemic myocardium, inducing angiogenesis, and negatively regulating cardiac fibroblast-myofibroblast transformation. This review provides an update on the known roles of Notch signaling in the mammalian heart. The goal is to assist in developing strategies to influence Notch signaling and optimize myocardial injury repair.