RESUMEN
PROBLEM: Is lipopolysaccharide (LPS) involved in the development of endometriosis? METHOD OF STUDY: BALB/c mice (n=69) were used for the murine endometriosis model. Mice with surgically induced endometriosis were injected with LPS intraperitoneally. After 4 weeks of LPS injections with or without the nuclear factor-kappa B (NF-κB) inhibitor, the extent of endometriosis-like lesions was evaluated. Expression of inflammatory factors in the implants was evaluated using real-time RT-PCR. Cell proliferation, angiogenic activity, inflammation, and NF-κB phosphorylation were assessed by immunohistochemical staining. RESULTS: Lipopolysaccharide increased total number, size, and mRNA expression of Ptgs-2, Vegf, Ccl-2, and Il-6 in endometriosis-like lesions. LPS also increased the percentage of Ki67-positive cells and enhanced the intensity and rate of positive cells of CD3, F4/80, and PECAM. Intense expression of phospho-NF-κB p65 after LPS administration was observed. Treatment with the NF-kB inhibitor negated these LPS-induced effects. CONCLUSION: LPS-induced pelvic inflammation status enhanced the development of murine endometriosis-like lesions via NF-κB pathway.
Asunto(s)
Endometriosis/patología , Lipopolisacáridos/toxicidad , FN-kappa B/metabolismo , Transducción de Señal/fisiología , Animales , Modelos Animales de Enfermedad , Endometriosis/metabolismo , Femenino , Inmunohistoquímica , Inflamación/inducido químicamente , Inflamación/metabolismo , Inflamación/patología , Ratones , Ratones Endogámicos BALB C , Reacción en Cadena en Tiempo Real de la Polimerasa , Transducción de Señal/efectos de los fármacosRESUMEN
The management of growth-restricted fetuses requires accurate diagnosis to optimize the timing of delivery. Doppler velocimetry is the only noninvasive method for assessing the fetoplacental hemodynamic status. This review will give a critical overview of the current knowledge on fetal venous blood flow in pregnancies complicated by in-trauterine growth-restricted fetuses. Adaptation of the circulation in intrauterine growth-restricted fetuses is described. Normal and abnormal venous Doppler waveforms are presented. Correlations of abnormal waveforms with the presence of acidemia and perinatal outcomes are emphasized. Limitations of venous Doppler velocimetry for optimizing the time for delivery and the perinatal outcome are also presented.
Asunto(s)
Retardo del Crecimiento Fetal/diagnóstico por imagen , Retardo del Crecimiento Fetal/fisiopatología , Ultrasonografía Doppler/métodos , Ultrasonografía Prenatal/métodos , Arterias Umbilicales/diagnóstico por imagen , Arterias Umbilicales/fisiopatología , Animales , Velocidad del Flujo Sanguíneo , Femenino , Humanos , Placenta/irrigación sanguínea , Placenta/diagnóstico por imagen , Valor Predictivo de las Pruebas , Embarazo , Resultado del Embarazo , Reología/métodosRESUMEN
Apoptosis is a distinctive form of programmed cell death resulting in the efficient elimination of cells without eliciting an inflammatory response. Endometriosis is characterized by the presence of endometrial cells with capacity to avoid apoptosis outside the uterus. Apoptosis plays a fundamental role for the pathogenesis of endometriosis. Eutopic endometrium from women with endometriosis has increased expression of anti-apoptotic factor and decreased expression of pro-apoptotic factors compared with endometrium from healthy women. These differences could contribute to the survival of regurgitating endometrial cells into the peritoneal cavity and development of endometriosis. Increased apoptosis of Fas-bearing immune cells in the peritoneal cavity may leads to their decreased scavenger activity that eventually results in prolonged survival of ectopic endometrial cells in women with endometriosis. This study is a current review of the literatures focused on the physiological role of apoptosis in normal endometrium and alterations in regulation of apoptosis in eutopic and ectopic endometrium from women with endometriosis. The role of apoptosis in the treatment of endometriosis is also reviewed.
Asunto(s)
Apoptosis/fisiología , Endometriosis/fisiopatología , Endometrio/metabolismo , Proteína Ligando Fas/metabolismo , Macrófagos Peritoneales/metabolismo , Mitocondrias/fisiología , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Endometriosis/tratamiento farmacológico , Endometriosis/metabolismo , Endometrio/citología , Endometrio/fisiología , Femenino , Humanos , Mitocondrias/metabolismoRESUMEN
Apigenin suppressed tumor necrosis factor α-induced cell proliferation and prostaglandin E2 expression via the attenuation of nuclear factor κB pathway in endometriotic stromal cells in vitro. Apigenin reduced the mitogenic activity and inflammatory reaction in endometriotic stromal cells.