Incremento de la expresión de Bax (proapoptótico) y disminución de la expresión de Bcl-2 (antiapoptótico) en recién nacidos con enterocolitis necrosante / Increase in pro-apoptotic Bax expression and decrease in anti-apoptotic Bcl-2 expression in newborns with necrotizing enterocolitis

Antecedentes/Objetivo: El objetivo de este estudio fue determinar si se producía un incremento de la expresión de Bax (proapoptótico) y una disminución de la expresión de Blc-2A1 (antiapoptótico) en el intestino de los recién nacidos con enterocolitis necrosante. Materiales y métodos: Comparamos a ocho pacientes recién nacidos de manera consecutiva sometidos a resección intestinal debido a enterocolitis necrosante con ocho recién nacidos sometidos a resección intestinal debido a atresia ileal. La evaluación histopatológica de la lesión tisular y la apoptosis se realizó mediante microscopía óptica y el método TUNEL. El nivel de ARNm en los genes apoptóticos (CASP3, CASP6, CASP7, Bax, BIRC2) y antiapoptóticos se evaluó con el método de matriz de RCP (PCR array). La expresión de proteínas se evaluó mediante inmunohistoquímica. Resultados: Los puntajes de las lesiones tisulares y los puntajes medios de apoptosis fueron significativamente más altos en el grupo con enterocolitis necrosante en comparación con el grupo de referencia (p < 0,01). La expresión de los genes proapoptóticos aumentó significativamente en el grupo con enterocolitis necrosante frente al grupo de referencia (p < 0,01). La expresión del gen Bcl-2A1 (antiapoptótico) disminuyó significativamente en el grupo con enterocolitis necrosante (p < 0,01). La expresión de las proteínas Bax y CASP3 aumentó significativamente en el grupo con enterocolitis necrosante (p < 0,01). Conclusión: Según nuestros datos, la alteración del equilibrio entre la expresión de Bax (proapoptótico) y la expresión de Bcl-2A1 (antiapoptótico) en el lugar de la lesión es un posible mecanismo de la patogenia en recién nacidos que presentan enterocolitis necrosante.

Background/Aim. The aim of the present study was to find out if there is an increase in the expression of pro-apoptotic Bax and reduction in expression of anti-apoptotic Blc-2A1 in newborn intestines with necrotizing enterocolitis (NEC). Material and Methods. We compared 8 consecutive newborn patients undergoing bowel resection for NEC with 8 neonates undergoing intestinal resection for ileal atresia. Histopathological evaluation of tissue injury and apoptosis was performed by using light microscopic examination and TUNEL method. The mRNA level of apoptotic (CASP3, CASP6, CASP7, Bax, BIRC2) and anti-apoptotic genes were evaluated by PCR array method. Protein expression was assessed by immunohistochemistry. Results. Tissue injury scores and mean apoptosis scores were significantly higher in NEC group when compared with control group (p <0.01). Expression of pro-apoptotic genes were significantly increased in NEC group when compared with control group (p <0.01). Expression of anti-apoptotic Bcl-2A1 gene was significantly decreased in NEC group, (p <0.01). Protein expression of Bax and CASP3 was significantly increased in NEC group, (p <0.01). Conclusion. Our data in humannewborns suggest that alteration of the balance between pro-apoptotic Bax expression and anti-apoptotic Bcl-2A1 expression in the site of injury is a possible mechanism in the pathogenesis of NEC.

Experimental study on the preventive mechanism of salviae miltiorrhizae against atherosclerosis in rabbits models / 华中科技大学学报（医学）（英德文版）

The preventive mechanism of salviae miltiorrhizae (SM) against experimental atherosclerosis (AS) in rabbits models was investigated. The experimental AS rabbit models were reproduced by feeding the high cholesterol diet. The changes of atherosclerotic plaques in normal group, model group and SM treated group were observed. The levels of serum TG, TC, HDL-C and LDL-C were determined. The immunohistochemistry was used to detect the expression of Bcl-2, Bax and IL-6 proteins in atherosclerotic plaques. The results showed that the level of serum TG in SM treated group was significantly lower than in model group (P<0.01). Immunohistochemistry revealed that the expression of Bcl-2, Bax and TL-6 in model group was significantly higher than in normal group. In the SM group, the expression of Bcl-2 protein was up-regulated and that of Bax was down-regulated. It was suggested that SM could inhibit formation of AS in experimental rabbits. To decrease the expression of Bax and increase the expression of Bcl-2 protein may be one of the mechanisms of SM against atherosclerosis.