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1.
Acta cir. bras ; 36(1): e360107, 2021. graf
Artículo en Inglés | LILACS | ID: biblio-1152691

RESUMEN

ABSTRACT Purpose The present study explored the potential therapeutic role of oleuropein in sepsis-induced heart injury along with the role of GSK-3β/NF-kB signaling pathway. Methods Sepsis-induced myocardial injury was induced by cecal ligation and puncture (CLP) in rats. The cardiac injury was assessed by measuring the levels of cTnI and creatine kinase-MB (CK-MB). Sepsis-induced inflammation was assessed by measuring interleukin-6 (IL-6), IL-10 and HMGB1 levels. The different doses of oleuropein (5, 10, and 20 mg/kg) were given prior to CLP. Oleuropein (20 mg/kg) was administered after 6 hof CLP. The expressions of GSK-3β, p-GSK-3β (Ser9) and nuclear factor-κB (NF-κB) were measured in heart homogenates. Results Cecal ligation and puncture was associated with myocardial injury, an increase in IL-6, a decrease in IL-10 and an increase in HMGB1. Moreover, it decreased the ratio of p-GSK-3β/GSK-3β and increased the expression of p-NF-kB. Pretreatment with oleuropein attenuated CLP-induced myocardial injury and systemic inflammation in a dose-dependent manner. Administration of oleuropein after the onset of CLP also attenuated cardiac injury and inflammation. It also restored CLP-induced changes in the HMGB1 levels, the ratio of p-GSK-3β/GSK-3β and expression of p- NF-kB. Conclusions Oleuropein attenuates sepsis-induced systemic inflammation and myocardial injury by inhibiting NF-kB and GSK-3β signaling.


Asunto(s)
Animales , Ratas , Sepsis/complicaciones , Sepsis/tratamiento farmacológico , Lesiones Cardíacas/tratamiento farmacológico , FN-kappa B , Iridoides , Glucósidos Iridoides , Glucógeno Sintasa Quinasa 3 beta
2.
Braz. j. med. biol. res ; 47(9): 766-772, 09/2014. tab, graf
Artículo en Inglés | LILACS | ID: lil-719315

RESUMEN

Cardiac contusion is a potentially fatal complication of blunt chest trauma. The effects of a combination of quercetin and methylprednisolone against trauma-induced cardiac contusion were studied. Thirty-five female Sprague-Dawley rats were divided into five groups (n=7) as follows: sham, cardiac contusion with no therapy, treated with methylprednisolone (30 mg/kg on the first day, and 3 mg/kg on the following days), treated with quercetin (50 mg·kg−1·day−1), and treated with a combination of methylprednisolone and quercetin. Serum troponin I (Tn-I) and tumor necrosis factor-alpha (TNF-α) levels and cardiac histopathological findings were evaluated. Tn-I and TNF-α levels were elevated after contusion (P=0.001 and P=0.001). Seven days later, Tn-I and TNF-α levels decreased in the rats treated with methylprednisolone, quercetin, and the combination of methylprednisolone and quercetin compared to the rats without therapy, but a statistical significance was found only with the combination therapy (P=0.001 and P=0.011, respectively). Histopathological degeneration and necrosis scores were statistically lower in the methylprednisolone and quercetin combination group compared to the group treated only with methylprednisolone (P=0.017 and P=0.007, respectively). However, only degeneration scores were lower in the combination therapy group compared to the group treated only with quercetin (P=0.017). Inducible nitric oxide synthase positivity scores were decreased in all treatment groups compared to the untreated groups (P=0.097, P=0.026, and P=0.004, respectively). We conclude that a combination of quercetin and methylprednisolone can be used for the specific treatment of cardiac contusion.


Asunto(s)
Animales , Femenino , Contusiones/tratamiento farmacológico , Lesiones Cardíacas/tratamiento farmacológico , Metilprednisolona/uso terapéutico , Miocardio/patología , Quercetina/uso terapéutico , Heridas no Penetrantes/complicaciones , Antiinflamatorios/uso terapéutico , Antioxidantes/uso terapéutico , Contusiones/etiología , Quimioterapia Combinada , Lesiones Cardíacas/etiología , Inmunohistoquímica , Necrosis , Óxido Nítrico Sintasa de Tipo II/aislamiento & purificación , Ratas Sprague-Dawley , Traumatismos Torácicos/complicaciones , Troponina I/sangre , Factor de Necrosis Tumoral alfa/sangre
3.
Cuad. cir ; 21(1): 75-83, 2007. tab, ilus
Artículo en Español | LILACS | ID: lil-489151

RESUMEN

Las primeras descripciones de una lesión cardiaca se remontan al papiro de Edwin Smith alrededor del 3000 AC. Hasta el siglo IX, las heridas penetrantes cardiacas eran consideradas intratables y mortales. Fue en 1896, cuando se reportó la primera reparación cardiaca exitosa. Aunque la mortalidad ha disminuido con el paso del tiempo, una herida penetrante al corazón sigue teniendo un grave pronóstico y es causa importante de morbilidad y mortalidad en pacientes de trauma. En la actualidad, cada vez se ven con más frecuencia las heridas penetrantes cardiacas por arma de fuego, lo que indudablemente ensombrece aún más el pronóstico de estas lesiones, por lo que se torna de vital importancia para el cirujano que trabaja en una Unidad de Emergencia, conocer con exactitud los mecanismos fisiopatológicos que se ven involucrados en este tipo de situaciones, además de todas las complicaciones que pueden ocurrir al intentar reparar una herida penetrante cardiaca. Este artículo pretende dar una visión precisa, clara y actual del manejo de un paciente con una herida penetrante cardiaca.


Asunto(s)
Humanos , Heridas Penetrantes/cirugía , Lesiones Cardíacas/cirugía , Lesiones Cardíacas/etiología , Adenosina/administración & dosificación , Antiarrítmicos/administración & dosificación , Urgencias Médicas , Heridas Penetrantes/fisiopatología , Heridas Penetrantes/tratamiento farmacológico , Lesiones Cardíacas/fisiopatología , Lesiones Cardíacas/tratamiento farmacológico , Complicaciones Posoperatorias , Resucitación , Toracotomía , Taponamiento Cardíaco/cirugía , Taponamiento Cardíaco/etiología
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