ABSTRACT
Abstract Systemic lupus erythematous (SLE) is an autoimmune disease with clinical manifestations in multiple organs, primarily striking women of reproductive age. Women with SLE can became pregnant such as any other healthy woman and carrier their pregnancy to term due to the improvement of health systems, but their specific inflammatory conditions could affect the microenvironment in which the fetus grows, and influence the development of placenta and the fetal heart. Until now, there is very little evidence of any increased risk of postnatal cardiovascular disease (CVD) in the apparently healthy children from women with SLE, but it is this great variability in the effects of lupus on pregnant products is related to.
Resumen El lupus eritematoso sistémico (LES) es una enfermedad autoinmune que presenta diversas manifestaciones clínicas en múltiples órganos, y afecta principalmente a mujeres en edad reproductiva. Las mujeres con LES se pueden embarazar y llevar a término su embarazo, sin embargo, las condiciones inflamatorias específicas de la madre pueden modificar el microambiente en el que el embrión y el feto se desarrollan y afectar la formación y desarrollo de la placenta y el corazón fetal. Hasta ahora hay muy poca evidencia de que haya un mayor riesgo de enfermedad cardiovascular (ECV) en hijos aparentemente sanos de madres con LES, a pesar de que se sabe que hay un mayor riesgo de alteraciones cognitivas y neuronales, así como de desarrollar enfermedades autoinmunes en esos niños. El objetivo de esta revisión fue realizar una búsqueda bibliografía cruzando palabras clave acerca la enfermedad cardiovascular en hijos sanos de mujeres con LES. La evidencia mostró que la autoinmunidad materna puede favorecer la predisposición para el desarrollo de ECV en sus hijos, por medio de la modificación de señales que alteran el microambiente durante la gestación, lo que puede afectar la respuesta inmunitaria y cambios epigenéticos durante la vida posnatal.
ABSTRACT
Aim: To observe the COX-2 pathway changes in hippocampus and cortex of rat offsprings following maternal inflammation during pregnancy. Methods: Female SD rats were randomly divided into control group and lipopolysaccharide (LPS) group. Rats in LPS group were intraperitonealy injected with LPS 300 μug · kg-1 on 11th, 14th and 18th day of pregnancy, while those in control group were given normal saline. Body weight of offspring rats on 3th, 10th, 20th and 30th day was recorded; on 30th day, the development of nervous system of the offspring rats was tested using water maze test, open field test and spontaneous activity test and so on; the histopathological changes of the hippocampus and cortex were detected by hematoxylineosin staining; the levels of inflammatory factors were measured by ELISA; the protein expression of COX-2 was measured by Western blot. Results: There were no significant differences in the body weight of offspring rats between NS group and LPS group (P >0. 05). In LPS group, it was found that the learning and memory function of rats were impaired, and horizontal movement and spontaneous activities were significantly reduced (P < 0. 05); the hippocampus and cortex neurons showed a significant nuclear pyknosis (P < 0. 05, P<0.01); the levels of PGD2, PGE2, PGI2, TNF- a, IL6 and IL-1 [J in hippocampus and cortex significantly increased (P < 0. 05, P < 0. 01); the protein expression of COX-2 in hippocampus and cortex significantly increased (P<0.01). Conclusions: COX-2 and downstream pathway are involved in the mechanism of brain injury in offsprings of pregnancy inflammation rats.