RESUMO
We investigated the molecular mechanisms responsible for fisetin-induced apoptosis in U266 cells. Fisetin elicited the cytotoxicity in U266 cells, manifested as an increased fraction of the cells with sub-G1 content or stained positively with TUNEL labeling. Fisetin enhanced caspase-3 activation, downregulation of Bcl-2 and Mcl-1(L), and upregulation of Bax, Bim and Bad. Fisetin activated AMPK as well as its substrate acetyl-CoA carboxylase (ACC), along with a decreased phosphorylation of AKT and mTOR. Fisetin also stimulated generation of ROS in U266 cells. Conversely, compound C or N-acetyl-L-cystein blocked fisetin-induced apoptosis. Our data suggest that fisetin-induced apoptosis in U266 cells is through ROS and AMPK pathways.
Assuntos
Proteínas Quinases Ativadas por AMP/metabolismo , Flavonoides/farmacologia , Mieloma Múltiplo/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral , Flavonóis , Humanos , Transdução de Sinais/efeitos dos fármacosRESUMO
Coronary artery stenosis is a major complication of Kawasaki disease (KD). Several interventional methods in treating coronary artery stenosis have been introduced. However, there are few reports on the management of in-stent restenosis after coronary stent implantation in children. Reported is a 10-year-old boy who underwent successful stent graft insertion for treating in-stent restenosis with neoaneurysm formation after stent implantation for severe coronary stenosis after KD. Twenty-eight months follow-up studies showed no significant restenosis and perfusion defect.
Assuntos
Implante de Prótese Vascular/instrumentação , Reestenose Coronária/etiologia , Reestenose Coronária/cirurgia , Síndrome de Linfonodos Mucocutâneos/complicações , Stents , Criança , Angiografia Coronária , Reestenose Coronária/diagnóstico , Seguimentos , Humanos , Masculino , Falha de Prótese , Reoperação , Tomografia Computadorizada de Emissão de Fóton ÚnicoRESUMO
BACKGROUND: Intraoperative transesophageal echocardiography and follow-up transthoracic echocardiography have been useful in assessing cardiac function in complete atrioventricular septal defects. However, it has been suggested that a discrepancy exists between intraoperative and postoperative findings, and that intraoperative findings cannot reliably predict long-term results. This study aims to determine whether this discrepancy exists and to assess whether it is possible to predict follow-up results using intraoperative transesophageal echocardiography. METHODS: A retrospective analysis was made in 35 patients who underwent biventricular repair by one surgeon between November 1997 and January 2004. All patients received intraoperative transesophageal echocardiography and follow-up transthoracic echocardiography at 19.1 +/- 18.02 months (range, 7 days to 5 years; median, 15.1 months). RESULTS: In left-sided atrioventricular valve regurgitation, 34.3% (12 of 35) of patients showed discrepancy during follow-up, and 28.6% (10 of 35) showed progression of regurgitation (from grade I to II). In right-sided atrioventricular valve, 11.4% (4 of 35) of patients showed discrepancy, 9.6% (3 of 35) showed progression of regurgitation (from grade I to II). CONCLUSIONS: In complete atrioventricular septal defects, intraoperative transesophageal echocardiography did not show the same findings as that of follow-up transthoracic echocardiography in some cases. However, this discrepancy is not so great as to require reoperation in early to midterm follow-up. Therefore, intraoperative transesophageal echocardiography may be used as tool to predict durability of surgical results and to decrease the incidence of reoperation in complete atrioventricular septal defects.